TY  - JOUR
AU  - Balint, Vanda
AU  - Perić, Mina
AU  - Dačić, Sanja
AU  - Stanisavljević Ninković, Danijela
AU  - Marjanović, Jelena
AU  - Popović, Jelena
AU  - Stevanović, Milena
AU  - Lazić, Andrijana
PY  - 2024
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2340
AB  - Astrocytes are the main homeostatic cells in the central nervous system, with the unique ability to transform from quiescent into a reactive state in response to pathological conditions by reacquiring some precursor properties. This process is known as reactive astrogliosis, a compensatory response that mediates tissue damage and recovery. Although it is well known that SOX transcription factors drive the expression of phenotype-specific genetic programs during neurodevelopment, their roles in mature astrocytes have not been studied extensively. We focused on the transcription factors SOX2 and SOX9, shown to be re-expressed in reactive astrocytes, in order to study the reactivation-related functional properties of astrocytes mediated by those proteins. We performed an initial screening of SOX2 and SOX9 expression after sensorimotor cortex ablation injury in rats and conducted gain-of-function studies in vitro using astrocytes derived from the human NT2/D1 cell line. Our results revealed the direct involvement of SOX2 in the reacquisition of proliferation in mature NT2/D1-derived astrocytes, while SOX9 overexpression increased migratory potential and glutamate uptake in these cells. Our results imply that modulation of SOX gene expression may change the functional properties of astrocytes, which holds promise for the discovery of potential therapeutic targets in the development of novel strategies for tissue regeneration and recovery.
PB  - MDPI
T2  - Biomedicines
T1  - The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes
IS  - 4
SP  - 796
VL  - 12
DO  - 10.3390/biomedicines12040796
ER  - 

@article{
author = "Balint, Vanda and Perić, Mina and Dačić, Sanja and Stanisavljević Ninković, Danijela and Marjanović, Jelena and Popović, Jelena and Stevanović, Milena and Lazić, Andrijana",
year = "2024",
abstract = "Astrocytes are the main homeostatic cells in the central nervous system, with the unique ability to transform from quiescent into a reactive state in response to pathological conditions by reacquiring some precursor properties. This process is known as reactive astrogliosis, a compensatory response that mediates tissue damage and recovery. Although it is well known that SOX transcription factors drive the expression of phenotype-specific genetic programs during neurodevelopment, their roles in mature astrocytes have not been studied extensively. We focused on the transcription factors SOX2 and SOX9, shown to be re-expressed in reactive astrocytes, in order to study the reactivation-related functional properties of astrocytes mediated by those proteins. We performed an initial screening of SOX2 and SOX9 expression after sensorimotor cortex ablation injury in rats and conducted gain-of-function studies in vitro using astrocytes derived from the human NT2/D1 cell line. Our results revealed the direct involvement of SOX2 in the reacquisition of proliferation in mature NT2/D1-derived astrocytes, while SOX9 overexpression increased migratory potential and glutamate uptake in these cells. Our results imply that modulation of SOX gene expression may change the functional properties of astrocytes, which holds promise for the discovery of potential therapeutic targets in the development of novel strategies for tissue regeneration and recovery.",
publisher = "MDPI",
journal = "Biomedicines",
title = "The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes",
number = "4",
pages = "796",
volume = "12",
doi = "10.3390/biomedicines12040796"
}

Balint, V., Perić, M., Dačić, S., Stanisavljević Ninković, D., Marjanović, J., Popović, J., Stevanović, M.,& Lazić, A.. (2024). The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes. in Biomedicines
MDPI., 12(4), 796.
https://doi.org/10.3390/biomedicines12040796

Balint V, Perić M, Dačić S, Stanisavljević Ninković D, Marjanović J, Popović J, Stevanović M, Lazić A. The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes. in Biomedicines. 2024;12(4):796.
doi:10.3390/biomedicines12040796 .

Balint, Vanda, Perić, Mina, Dačić, Sanja, Stanisavljević Ninković, Danijela, Marjanović, Jelena, Popović, Jelena, Stevanović, Milena, Lazić, Andrijana, "The Role of SOX2 and SOX9 Transcription Factors in the Reactivation-Related Functional Properties of NT2/D1-Derived Astrocytes" in Biomedicines, 12, no. 4 (2024):796,
https://doi.org/10.3390/biomedicines12040796 . .

TY  - JOUR
AU  - Radmilović, Mihajlo D.
AU  - Drvenica, Ivana T.
AU  - Rabasović, Mihailo D.
AU  - Ilić, Vesna Lj.
AU  - Pavlović, Danica
AU  - Oasa, Sho
AU  - Vukojević, Vladana
AU  - Perić, Mina
AU  - Nikolić, Stanko N.
AU  - Krmpot, Aleksandar J.
PY  - 2023
UR  - https://www.sciencedirect.com/science/article/pii/S0141813023022067
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2288
AB  - Hemoglobin (Hb), a life-sustaining and highly abundant erythrocyte protein, is not readily fluorescent. A few studies have already reported Two-Photon Excited Fluorescence (TPEF) of Hb, however, the mechanisms through which Hb becomes fluorescent upon interaction with ultrashort laser pulses are not completely understood. Here, we characterized photophysically this interaction on Hb thin film and erythrocytes using fluorescence spectroscopy upon single-photon/two-photon absorption, and UV-VIS single-photon absorption spectroscopy. A gradual increase of the fluorescence intensity, ending up with saturation, is observed upon prolonged exposure of Hb thin layer and erythrocytes to ultrashort laser pulses at 730 nm. When compared to protoporphyrin IX (PpIX) and oxidized Hb by H2O2, TPEF spectra from a thin Hb film and erythrocytes showed good mutual agreement, broad peaking at 550 nm, supporting hemoglobin undergoes degradation and that same fluorescent specie(s) originating from the heme moiety are generated. The uniform square shaped patterns of the fluorescent photoproduct exhibited the same level of the fluorescence intensity even after 12 weeks from the formation, indicating high photoproduct stability. We finally demonstrated the full potential of the formed Hb photoproduct with TPEF scanning microscopy towards spatiotemporally controlled micropatterning in HTF and single human erythrocyte labelling and tracking in the whole blood.
PB  - Elsevier
T2  - International Journal of Biological Macromolecules
T1  - Interactions of ultrashort laser pulses with hemoglobin: Photophysical aspects and potential applications
SP  - 125312
VL  - 244
DO  - 10.1016/j.ijbiomac.2023.125312
ER  - 

@article{
author = "Radmilović, Mihajlo D. and Drvenica, Ivana T. and Rabasović, Mihailo D. and Ilić, Vesna Lj. and Pavlović, Danica and Oasa, Sho and Vukojević, Vladana and Perić, Mina and Nikolić, Stanko N. and Krmpot, Aleksandar J.",
year = "2023",
abstract = "Hemoglobin (Hb), a life-sustaining and highly abundant erythrocyte protein, is not readily fluorescent. A few studies have already reported Two-Photon Excited Fluorescence (TPEF) of Hb, however, the mechanisms through which Hb becomes fluorescent upon interaction with ultrashort laser pulses are not completely understood. Here, we characterized photophysically this interaction on Hb thin film and erythrocytes using fluorescence spectroscopy upon single-photon/two-photon absorption, and UV-VIS single-photon absorption spectroscopy. A gradual increase of the fluorescence intensity, ending up with saturation, is observed upon prolonged exposure of Hb thin layer and erythrocytes to ultrashort laser pulses at 730 nm. When compared to protoporphyrin IX (PpIX) and oxidized Hb by H2O2, TPEF spectra from a thin Hb film and erythrocytes showed good mutual agreement, broad peaking at 550 nm, supporting hemoglobin undergoes degradation and that same fluorescent specie(s) originating from the heme moiety are generated. The uniform square shaped patterns of the fluorescent photoproduct exhibited the same level of the fluorescence intensity even after 12 weeks from the formation, indicating high photoproduct stability. We finally demonstrated the full potential of the formed Hb photoproduct with TPEF scanning microscopy towards spatiotemporally controlled micropatterning in HTF and single human erythrocyte labelling and tracking in the whole blood.",
publisher = "Elsevier",
journal = "International Journal of Biological Macromolecules",
title = "Interactions of ultrashort laser pulses with hemoglobin: Photophysical aspects and potential applications",
pages = "125312",
volume = "244",
doi = "10.1016/j.ijbiomac.2023.125312"
}

Radmilović, M. D., Drvenica, I. T., Rabasović, M. D., Ilić, V. Lj., Pavlović, D., Oasa, S., Vukojević, V., Perić, M., Nikolić, S. N.,& Krmpot, A. J.. (2023). Interactions of ultrashort laser pulses with hemoglobin: Photophysical aspects and potential applications. in International Journal of Biological Macromolecules
Elsevier., 244, 125312.
https://doi.org/10.1016/j.ijbiomac.2023.125312

Radmilović MD, Drvenica IT, Rabasović MD, Ilić VL, Pavlović D, Oasa S, Vukojević V, Perić M, Nikolić SN, Krmpot AJ. Interactions of ultrashort laser pulses with hemoglobin: Photophysical aspects and potential applications. in International Journal of Biological Macromolecules. 2023;244:125312.
doi:10.1016/j.ijbiomac.2023.125312 .

Radmilović, Mihajlo D., Drvenica, Ivana T., Rabasović, Mihailo D., Ilić, Vesna Lj., Pavlović, Danica, Oasa, Sho, Vukojević, Vladana, Perić, Mina, Nikolić, Stanko N., Krmpot, Aleksandar J., "Interactions of ultrashort laser pulses with hemoglobin: Photophysical aspects and potential applications" in International Journal of Biological Macromolecules, 244 (2023):125312,
https://doi.org/10.1016/j.ijbiomac.2023.125312 . .

TY  - CONF
AU  - Balint, Vanda
AU  - Stanisavljević-Ninković, Danijela
AU  - Lazić, Stefan
AU  - Kovačević-Grujičić, Nataša
AU  - Perić, Mina
AU  - Pejić, Jelena
AU  - Mojsin, Marija
AU  - Stevanović, Milena
AU  - Lazić, Andrijana
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2185
AB  - Astrocytes are the main homeostatic cells in the brain with important roles both in
physiological and pathological conditions. They have a unique ability to become
reactivated in response to different types of brain pathologies, which serves as a
compensatory response that modulates tissue damage and recovery. Also, senescent
astrocytes have profound implications in age-related neurodegenerative disorders. The
molecular mechanisms underlying astrocyte reactivation and senescence are still not
well understood. To investigate the roles of SOX2 and SOX9 transcription factors and
miR-21 in these phenotypic alternations of astroglia, astrocytes derived from NT2/D1
cell line (NT2/A) were used as a model system. Western blot analyses showed that the
expression of both SOX2 and SOX9 decreases during the maturation of NT2/A and
they are re-expressed upon in vitro induced injury. Further modulation of the SOX2
and SOX9 expression will reveal their roles in the regulation of astrocytes
reactivation. Down-regulation of mir-21 in both immature and mature NT2/A by
using the antisense technology, induced the decline in cell proliferation revealed by
Ki67 proliferation marker. Also the premature cellular senescence was induced as
indicated by increase in SA-ß-gal activity and the expression of p21 and p53.
Additionally, in silico analysis predicted many of the genes, previously shown to be
upregulated in senescent astrocytes, as miR-21 targets.
Clarifying the roles of SOX genes and miRNAs in astrocyte reactivation and
senescence would contribute to better understanding of the functions of these cells at
the molecular level, which holds promise for development of new therapeutic
strategies.
PB  - Belgrade : Serbian Neuroscience Society
C3  - 8th Congress of the Serbian Neuroscience Society
T1  - The role of specific SOX genes and microRNAs in reactivation and senescence of human astrocytes derived from pluripotent NT2/D1 cells
EP  - 99
SP  - 99
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2185
ER  - 

@conference{
author = "Balint, Vanda and Stanisavljević-Ninković, Danijela and Lazić, Stefan and Kovačević-Grujičić, Nataša and Perić, Mina and Pejić, Jelena and Mojsin, Marija and Stevanović, Milena and Lazić, Andrijana",
year = "2023",
abstract = "Astrocytes are the main homeostatic cells in the brain with important roles both in
physiological and pathological conditions. They have a unique ability to become
reactivated in response to different types of brain pathologies, which serves as a
compensatory response that modulates tissue damage and recovery. Also, senescent
astrocytes have profound implications in age-related neurodegenerative disorders. The
molecular mechanisms underlying astrocyte reactivation and senescence are still not
well understood. To investigate the roles of SOX2 and SOX9 transcription factors and
miR-21 in these phenotypic alternations of astroglia, astrocytes derived from NT2/D1
cell line (NT2/A) were used as a model system. Western blot analyses showed that the
expression of both SOX2 and SOX9 decreases during the maturation of NT2/A and
they are re-expressed upon in vitro induced injury. Further modulation of the SOX2
and SOX9 expression will reveal their roles in the regulation of astrocytes
reactivation. Down-regulation of mir-21 in both immature and mature NT2/A by
using the antisense technology, induced the decline in cell proliferation revealed by
Ki67 proliferation marker. Also the premature cellular senescence was induced as
indicated by increase in SA-ß-gal activity and the expression of p21 and p53.
Additionally, in silico analysis predicted many of the genes, previously shown to be
upregulated in senescent astrocytes, as miR-21 targets.
Clarifying the roles of SOX genes and miRNAs in astrocyte reactivation and
senescence would contribute to better understanding of the functions of these cells at
the molecular level, which holds promise for development of new therapeutic
strategies.",
publisher = "Belgrade : Serbian Neuroscience Society",
journal = "8th Congress of the Serbian Neuroscience Society",
title = "The role of specific SOX genes and microRNAs in reactivation and senescence of human astrocytes derived from pluripotent NT2/D1 cells",
pages = "99-99",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2185"
}

Balint, V., Stanisavljević-Ninković, D., Lazić, S., Kovačević-Grujičić, N., Perić, M., Pejić, J., Mojsin, M., Stevanović, M.,& Lazić, A.. (2023). The role of specific SOX genes and microRNAs in reactivation and senescence of human astrocytes derived from pluripotent NT2/D1 cells. in 8th Congress of the Serbian Neuroscience Society
Belgrade : Serbian Neuroscience Society., 99-99.
https://hdl.handle.net/21.15107/rcub_imagine_2185

Balint V, Stanisavljević-Ninković D, Lazić S, Kovačević-Grujičić N, Perić M, Pejić J, Mojsin M, Stevanović M, Lazić A. The role of specific SOX genes and microRNAs in reactivation and senescence of human astrocytes derived from pluripotent NT2/D1 cells. in 8th Congress of the Serbian Neuroscience Society. 2023;:99-99.
https://hdl.handle.net/21.15107/rcub_imagine_2185 .

Balint, Vanda, Stanisavljević-Ninković, Danijela, Lazić, Stefan, Kovačević-Grujičić, Nataša, Perić, Mina, Pejić, Jelena, Mojsin, Marija, Stevanović, Milena, Lazić, Andrijana, "The role of specific SOX genes and microRNAs in reactivation and senescence of human astrocytes derived from pluripotent NT2/D1 cells" in 8th Congress of the Serbian Neuroscience Society (2023):99-99,
https://hdl.handle.net/21.15107/rcub_imagine_2185 .

TY  - CONF
AU  - Simeunović, Ivana
AU  - Čuturilo, Goran
AU  - Kovačević-Grujičić, Nataša
AU  - Petter, Olena
AU  - Perić, Mina
AU  - Kostić, Jovana
AU  - Harwood J., Adrian
AU  - Stevanović, Milena
AU  - Drakulić, Danijela
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2138
AB  - Introduction: Neurodevelopmental disorders (NDDs), such as autism spectrum disorders (ASD), intellectual disability (ID),schizophrenia, and bipolar disorder, are caused by the alterationsin early brain development. They affect approximately 4% of the European population and represent a high
socio-economic impact and financial burden. Treatments of NDDs are focused on symptoms since molecular mechanisms underlying NDDs are still unknown. One of the syndromes with a high risk for NDDs
is 22q11.2 Deletion Syndrome (22q11.2DS) caused by microdeletion 22q11.2. 22q11.2 microdeletion is
the most common microdeletion in humans; it is one of the strongest known risk factorsfor development
of psychiatric illness and the highest known genetic risk for schizophrenia (approximately, 25% of patients with 22q11.2DS develop schizophrenia compared to 1% in the general population).
Methods: Genomic and clinical findings in 35 patients with 22q11.2DS were analyzed and peripheral
blood mononuclear cells of patients with 22q11.2DS and healthy controls were reprogrammed.
Results: The majority of patients have 3 Mb deletion and nine of them have inherited 22q11.2 microdeletion from parents. Twenty-one different clinical presentations are revealed in the cohort with developmental delay detected in about 50% of patients. iPSCs were generated from four patients with
22q11.2 microdeletion and five healthy controls.
Conclusion: Cohort of patients with 22q11.2DS isform and iPSCs were generated which enable research
of molecular mechanisms underlying NDDs.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Generation of induced pluripotent stem cells derived from patients with 22q11.2 deletion syndrome as a tool for studying neurodevelopmental disorders
EP  - 84
SP  - 84
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2138
ER  - 

@conference{
author = "Simeunović, Ivana and Čuturilo, Goran and Kovačević-Grujičić, Nataša and Petter, Olena and Perić, Mina and Kostić, Jovana and Harwood J., Adrian and Stevanović, Milena and Drakulić, Danijela",
year = "2023",
abstract = "Introduction: Neurodevelopmental disorders (NDDs), such as autism spectrum disorders (ASD), intellectual disability (ID),schizophrenia, and bipolar disorder, are caused by the alterationsin early brain development. They affect approximately 4% of the European population and represent a high
socio-economic impact and financial burden. Treatments of NDDs are focused on symptoms since molecular mechanisms underlying NDDs are still unknown. One of the syndromes with a high risk for NDDs
is 22q11.2 Deletion Syndrome (22q11.2DS) caused by microdeletion 22q11.2. 22q11.2 microdeletion is
the most common microdeletion in humans; it is one of the strongest known risk factorsfor development
of psychiatric illness and the highest known genetic risk for schizophrenia (approximately, 25% of patients with 22q11.2DS develop schizophrenia compared to 1% in the general population).
Methods: Genomic and clinical findings in 35 patients with 22q11.2DS were analyzed and peripheral
blood mononuclear cells of patients with 22q11.2DS and healthy controls were reprogrammed.
Results: The majority of patients have 3 Mb deletion and nine of them have inherited 22q11.2 microdeletion from parents. Twenty-one different clinical presentations are revealed in the cohort with developmental delay detected in about 50% of patients. iPSCs were generated from four patients with
22q11.2 microdeletion and five healthy controls.
Conclusion: Cohort of patients with 22q11.2DS isform and iPSCs were generated which enable research
of molecular mechanisms underlying NDDs.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Generation of induced pluripotent stem cells derived from patients with 22q11.2 deletion syndrome as a tool for studying neurodevelopmental disorders",
pages = "84-84",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2138"
}

Simeunović, I., Čuturilo, G., Kovačević-Grujičić, N., Petter, O., Perić, M., Kostić, J., Harwood J., A., Stevanović, M.,& Drakulić, D.. (2023). Generation of induced pluripotent stem cells derived from patients with 22q11.2 deletion syndrome as a tool for studying neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 84-84.
https://hdl.handle.net/21.15107/rcub_imagine_2138

Simeunović I, Čuturilo G, Kovačević-Grujičić N, Petter O, Perić M, Kostić J, Harwood J. A, Stevanović M, Drakulić D. Generation of induced pluripotent stem cells derived from patients with 22q11.2 deletion syndrome as a tool for studying neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:84-84.
https://hdl.handle.net/21.15107/rcub_imagine_2138 .

Simeunović, Ivana, Čuturilo, Goran, Kovačević-Grujičić, Nataša, Petter, Olena, Perić, Mina, Kostić, Jovana, Harwood J., Adrian, Stevanović, Milena, Drakulić, Danijela, "Generation of induced pluripotent stem cells derived from patients with 22q11.2 deletion syndrome as a tool for studying neurodevelopmental disorders" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):84-84,
https://hdl.handle.net/21.15107/rcub_imagine_2138 .

TY  - CONF
AU  - Kostić, Jovana
AU  - Drakulić, Danijela
AU  - Čuturilo, Goran
AU  - Petter, Olena
AU  - Perić, Mina
AU  - Simeunović, Ivana
AU  - Harwood J., Adrian
AU  - Stevanović, Milena
AU  - Kovačević-Grujičić, Nataša
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2122
AB  - Introduction: Neurodevelopmental disorders (NDDs), such as autism spectrum disorders (ASD), schizophrenia, and intellectual disability, represent important public health challenge in modern societies
with a prevalence of about 10 to 15% of all births and the tendency of increasing worldwide. They are
caused by disruption of early brain development. Treatments of NDDs are focused on symptoms due to
a limited understanding of underlying pathophysiological mechanisms. Individuals with the 22q11.2
Duplication Syndrome (22q11.2dup), caused by heterozygous 22q11.2 microduplication, have an elevated risk of developing NDDs. Literature data revealed that ASD is detected in 14-25% of patients with
22q11.2dup while schizophrenia is less common in these patients than in the general population, suggesting that 22q11.2 duplication might be protective against schizophrenia.
Methods: Genomic and clinical findingsin patients with 22q11.2dup were analyzed and peripheral blood
mononuclear cells of patients with 22q11.2dup were reprogrammed.
Results: We formed a cohort of 8 patients with 22q11.2dup. The majority of patientsin our cohort have
microduplication of approximately 3Mb (80%). Also, the majority of them are familial cases and in 67%
of cases, the 22q11.2 microduplication is inherited from the mother. Congenital heart defects were detected in 25% of our patients, while all tested patients have facial dysmorphism. iPSCs were generated
from three patients with a familial form of 22q11.2dup and their mothers.
Conclusion: A cohort of patients with 22q11.2dup is formed and iPSCs were generated which can be
used as a model system for studying NDDs.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - Establishment of induced pluripotent stem cells from patients with 22q11.2 duplication syndrome as a model system for studying neurodevelopmental disorders
EP  - 66
SP  - 66
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2122
ER  - 

@conference{
author = "Kostić, Jovana and Drakulić, Danijela and Čuturilo, Goran and Petter, Olena and Perić, Mina and Simeunović, Ivana and Harwood J., Adrian and Stevanović, Milena and Kovačević-Grujičić, Nataša",
year = "2023",
abstract = "Introduction: Neurodevelopmental disorders (NDDs), such as autism spectrum disorders (ASD), schizophrenia, and intellectual disability, represent important public health challenge in modern societies
with a prevalence of about 10 to 15% of all births and the tendency of increasing worldwide. They are
caused by disruption of early brain development. Treatments of NDDs are focused on symptoms due to
a limited understanding of underlying pathophysiological mechanisms. Individuals with the 22q11.2
Duplication Syndrome (22q11.2dup), caused by heterozygous 22q11.2 microduplication, have an elevated risk of developing NDDs. Literature data revealed that ASD is detected in 14-25% of patients with
22q11.2dup while schizophrenia is less common in these patients than in the general population, suggesting that 22q11.2 duplication might be protective against schizophrenia.
Methods: Genomic and clinical findingsin patients with 22q11.2dup were analyzed and peripheral blood
mononuclear cells of patients with 22q11.2dup were reprogrammed.
Results: We formed a cohort of 8 patients with 22q11.2dup. The majority of patientsin our cohort have
microduplication of approximately 3Mb (80%). Also, the majority of them are familial cases and in 67%
of cases, the 22q11.2 microduplication is inherited from the mother. Congenital heart defects were detected in 25% of our patients, while all tested patients have facial dysmorphism. iPSCs were generated
from three patients with a familial form of 22q11.2dup and their mothers.
Conclusion: A cohort of patients with 22q11.2dup is formed and iPSCs were generated which can be
used as a model system for studying NDDs.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "Establishment of induced pluripotent stem cells from patients with 22q11.2 duplication syndrome as a model system for studying neurodevelopmental disorders",
pages = "66-66",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2122"
}

Kostić, J., Drakulić, D., Čuturilo, G., Petter, O., Perić, M., Simeunović, I., Harwood J., A., Stevanović, M.,& Kovačević-Grujičić, N.. (2023). Establishment of induced pluripotent stem cells from patients with 22q11.2 duplication syndrome as a model system for studying neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 66-66.
https://hdl.handle.net/21.15107/rcub_imagine_2122

Kostić J, Drakulić D, Čuturilo G, Petter O, Perić M, Simeunović I, Harwood J. A, Stevanović M, Kovačević-Grujičić N. Establishment of induced pluripotent stem cells from patients with 22q11.2 duplication syndrome as a model system for studying neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:66-66.
https://hdl.handle.net/21.15107/rcub_imagine_2122 .

Kostić, Jovana, Drakulić, Danijela, Čuturilo, Goran, Petter, Olena, Perić, Mina, Simeunović, Ivana, Harwood J., Adrian, Stevanović, Milena, Kovačević-Grujičić, Nataša, "Establishment of induced pluripotent stem cells from patients with 22q11.2 duplication syndrome as a model system for studying neurodevelopmental disorders" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):66-66,
https://hdl.handle.net/21.15107/rcub_imagine_2122 .

TY  - CONF
AU  - Lazić, Adrijana
AU  - Drakulić, Danijela
AU  - Kovačević-Grujičić, Nataša
AU  - Perić, Mina
AU  - Petrakis, Spyros
AU  - Linden, David
AU  - Harwood, Adrian
AU  - Stevanović, Milena
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2110
AB  - Introduction: Neurodevelopmental disorders (NDDs) are a group of complex and heterogeneous disorders that include autism spectrum disorders, intellectual disability, schizophrenia and bipolar disorder. However, underlying pathophysiological mechanisms are mostly unknown. In order to get better understanding of the underlying mechanisms and to discover potential therapeutics we have focused our research on 22q11.2 Deletion Syndrome (22q11.2DS), caused by microdeletion of the region q11.2 of chromosome 22 and associated with a high risk for NDDs. Methods: To study molecular mechanisms underlying intrafamilial phenotypic variability, we have identified families with the inherited form of 22q11.2DS with the aim of conducting the following analyses: whole genome sequencing in order to detect additional genetic variation(s) present in the affected child; generation of induced pluripotent stem cells (iPSCs) from peripheral blood mononuclear cells; analysis of the effects of 22q11.2 microdeletion on neural differentiation including organoids as 3D model system; transcriptome analysis of iPSC-derived neurons and astrocytesto determine differentially expressed gene sets and dysregulated pathways; and testing the metabolic changes and drug responsiveness of neurons and astrocytes by high-throughput cell-based assays. Results: Peripheral blood mononuclear cells of the families with inherited form of 22q11.2DS were reprogrammed and established iPSCs were characterized. Generated iPSCs will be subjected to the further analyses. Conclusion: Currently, most of the treatments of NDDs are symptom-based due to limited understanding of underlying pathophysiological mechanisms. It is expected that patient-derived iPSCs will enable a deeper understanding of unique disease mechanisms and may also provide a significant contribution in preclinical drug development.
PB  - Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade
C3  - CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
T1  - 22q11.2 Deletion syndrome as a tool for modelling and research of neurodevelopmental disorders
EP  - 31
SP  - 31
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2110
ER  - 

@conference{
author = "Lazić, Adrijana and Drakulić, Danijela and Kovačević-Grujičić, Nataša and Perić, Mina and Petrakis, Spyros and Linden, David and Harwood, Adrian and Stevanović, Milena",
year = "2023",
abstract = "Introduction: Neurodevelopmental disorders (NDDs) are a group of complex and heterogeneous disorders that include autism spectrum disorders, intellectual disability, schizophrenia and bipolar disorder. However, underlying pathophysiological mechanisms are mostly unknown. In order to get better understanding of the underlying mechanisms and to discover potential therapeutics we have focused our research on 22q11.2 Deletion Syndrome (22q11.2DS), caused by microdeletion of the region q11.2 of chromosome 22 and associated with a high risk for NDDs. Methods: To study molecular mechanisms underlying intrafamilial phenotypic variability, we have identified families with the inherited form of 22q11.2DS with the aim of conducting the following analyses: whole genome sequencing in order to detect additional genetic variation(s) present in the affected child; generation of induced pluripotent stem cells (iPSCs) from peripheral blood mononuclear cells; analysis of the effects of 22q11.2 microdeletion on neural differentiation including organoids as 3D model system; transcriptome analysis of iPSC-derived neurons and astrocytesto determine differentially expressed gene sets and dysregulated pathways; and testing the metabolic changes and drug responsiveness of neurons and astrocytes by high-throughput cell-based assays. Results: Peripheral blood mononuclear cells of the families with inherited form of 22q11.2DS were reprogrammed and established iPSCs were characterized. Generated iPSCs will be subjected to the further analyses. Conclusion: Currently, most of the treatments of NDDs are symptom-based due to limited understanding of underlying pathophysiological mechanisms. It is expected that patient-derived iPSCs will enable a deeper understanding of unique disease mechanisms and may also provide a significant contribution in preclinical drug development.",
publisher = "Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade",
journal = "CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia",
title = "22q11.2 Deletion syndrome as a tool for modelling and research of neurodevelopmental disorders",
pages = "31-31",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2110"
}

Lazić, A., Drakulić, D., Kovačević-Grujičić, N., Perić, M., Petrakis, S., Linden, D., Harwood, A.,& Stevanović, M.. (2023). 22q11.2 Deletion syndrome as a tool for modelling and research of neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia
Institute of Molecular Genetics and Genetic Engineering (IMGGE), University of Belgrade., 31-31.
https://hdl.handle.net/21.15107/rcub_imagine_2110

Lazić A, Drakulić D, Kovačević-Grujičić N, Perić M, Petrakis S, Linden D, Harwood A, Stevanović M. 22q11.2 Deletion syndrome as a tool for modelling and research of neurodevelopmental disorders. in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia. 2023;:31-31.
https://hdl.handle.net/21.15107/rcub_imagine_2110 .

Lazić, Adrijana, Drakulić, Danijela, Kovačević-Grujičić, Nataša, Perić, Mina, Petrakis, Spyros, Linden, David, Harwood, Adrian, Stevanović, Milena, "22q11.2 Deletion syndrome as a tool for modelling and research of neurodevelopmental disorders" in CoMBoS2 – the Second Congress of Molecular Biologists of Serbia, Abstract Book – Trends in Molecular Biology, Special issue 06-08 October 2023, Belgrade, Serbia (2023):31-31,
https://hdl.handle.net/21.15107/rcub_imagine_2110 .

TY  - THES
AU  - Perić, Mina
PY  - 2022
UR  - https://eteze.bg.ac.rs/application/showtheses?thesesId=8761
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:26789/bdef:Content/download
UR  - https://nardus.mpn.gov.rs/handle/123456789/20773
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/66
AB  - Amiotrofična lateralna skleroza (ALS) je neurodegenerativna bolest koju karakteriše smrt motornih neurona u kičmenoj moždini i mozgu. Iako su neuroni pogođeni u ALS, glijske ćelije imaju značajnu ulogu u nastanku i progresiji bolesti. Ćelije glije doprinose održavanju homeostaze K+ u vanćelijskoj sredini, a posebno važnu ulogu ima ulazni ispravljački kalijumov kanal Kir4.1 koji je u velikoj meri eksprimiran u astrocitima i oligodendrocitima. Prethodne studije su pokazale narušenu ekspresiju i funkciju Kir4.1 u astrocitima u ALS, a u ovoj studiji je ispitivana uloga Kir4.1 u oligodendrocitima na hSOD1G93A modelu pacova primenom imunofluorescencije, konfokalne mikroskopije, Western blot-a i elektrofiziologije na deliću membrane. Rezultati ove studije pokazali su da je kod ALS životinja smanjena ekspresija Kir4.1 u oligodendrocitima u kičmenoj moždini, kao i u njenoj mijelinskoj frakciji. Nađeno je i da su u ALS oligodendrocitima u kulturi membranske biofizičke osobine narušene, a struje kroz Kir kanale smanjene, ukazujući na narušena funkcionalna svojstva ovih glijskih ćelija. Iako je ukupna ekspresija Kir4.1 smanjena u ALS, uočeni su izolovani regioni u ventralnim rogovima hSOD1G93A kičmene moždine koji zadržavaju Kir4.1 imunoreaktivnost u okviru specifičnih klastera mikroglije. Zapaženo je da se Kir4.1+ klasteri mikroglije preklapaju sa regionima izraženog prisustva proteinskih agregata mutirane superoksid dismutaze 1, kao osnovnog obeležja ALS. Membranske biofizičke osobine neonatalne mikroglije i aktivnost Kir kanala nisu narušeni u ALS dok adultna ALS mikroglija u kulturi pokazuje smanjenje Kir struja. Promene u ekspresiji Kir4.1 ističu doprinos ovog kalijumovog kanala neurodegenerativnim procesima i ukazuju na njegov potencijalni značaj za ciljanu terapiju ALS.
AB  - Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the death of motor neurons in the spinal cord and brain. Although neurons are affected in ALS, glial cells play an important role in the disease onset and progression. Glial cells contribute to the maintenance of extracellular K+ homeostasis through the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in astrocytes and oligodendrocytes. Previous studies demonstrated impaired expression and function of Kir4.1 in astrocytes in ALS. Therefore, we first examined the role of Kir4.1 in spinal cord oligodendrocytes of the hSOD1G93A rat model by employing immunofluorescence, confocal microscopy, Western blot, and patch-clamp. We show reduced expression of Kir4.1 in oligodendrocytes in the ALS spinal cord as well as in its myelin fraction. Oligodendrocytes in culture display impaired membrane biophysical properties and decreased Kir currents, indicating their compromised functional properties. Although the expression of Kir4.1 was diminished in ALS, we observed isolated regions retaining Kir4.1 immunoreactivity in ventral horns of the hSOD1G93A spinal cord that contained cell clusters enriched in microglia. Our data show that Kir4.1+ clusters of microglia overlap with regions of pronounced presence of protein aggregates of mutated superoxide dismutase 1 that represent the hallmark of ALS. Membrane biophysical properties and Kir channel activity were not altered in neonatal ALS microglia while adult ALS microglia in culture displayed reduced Kir currents. Changes in the expression and function of Kir4.1 highlight the importance of this potassium channel in neurodegeneration suggesting Kir4.1 as a potential therapeutic target in ALS pathology.
PB  - Univerzitet u Beogradu, Biološki fakultet
T1  - Neurodegenerativne promene u ćelijama glije, oligodendrocitima i mikrogliji, u kičmenoj moždini na pacovskom hsod1g93a modelu amiotrofične lateralne skleroze
T1  - Neurodegenerative changes in glial cells, oligodendrocytes and microglia in the spinal cord of hsod1g93a rat model of amyotrophic lateral sclerosis
UR  - https://hdl.handle.net/21.15107/rcub_nardus_20773
ER  - 

@phdthesis{
author = "Perić, Mina",
year = "2022",
abstract = "Amiotrofična lateralna skleroza (ALS) je neurodegenerativna bolest koju karakteriše smrt motornih neurona u kičmenoj moždini i mozgu. Iako su neuroni pogođeni u ALS, glijske ćelije imaju značajnu ulogu u nastanku i progresiji bolesti. Ćelije glije doprinose održavanju homeostaze K+ u vanćelijskoj sredini, a posebno važnu ulogu ima ulazni ispravljački kalijumov kanal Kir4.1 koji je u velikoj meri eksprimiran u astrocitima i oligodendrocitima. Prethodne studije su pokazale narušenu ekspresiju i funkciju Kir4.1 u astrocitima u ALS, a u ovoj studiji je ispitivana uloga Kir4.1 u oligodendrocitima na hSOD1G93A modelu pacova primenom imunofluorescencije, konfokalne mikroskopije, Western blot-a i elektrofiziologije na deliću membrane. Rezultati ove studije pokazali su da je kod ALS životinja smanjena ekspresija Kir4.1 u oligodendrocitima u kičmenoj moždini, kao i u njenoj mijelinskoj frakciji. Nađeno je i da su u ALS oligodendrocitima u kulturi membranske biofizičke osobine narušene, a struje kroz Kir kanale smanjene, ukazujući na narušena funkcionalna svojstva ovih glijskih ćelija. Iako je ukupna ekspresija Kir4.1 smanjena u ALS, uočeni su izolovani regioni u ventralnim rogovima hSOD1G93A kičmene moždine koji zadržavaju Kir4.1 imunoreaktivnost u okviru specifičnih klastera mikroglije. Zapaženo je da se Kir4.1+ klasteri mikroglije preklapaju sa regionima izraženog prisustva proteinskih agregata mutirane superoksid dismutaze 1, kao osnovnog obeležja ALS. Membranske biofizičke osobine neonatalne mikroglije i aktivnost Kir kanala nisu narušeni u ALS dok adultna ALS mikroglija u kulturi pokazuje smanjenje Kir struja. Promene u ekspresiji Kir4.1 ističu doprinos ovog kalijumovog kanala neurodegenerativnim procesima i ukazuju na njegov potencijalni značaj za ciljanu terapiju ALS., Amyotrophic lateral sclerosis (ALS) is a neurodegenerative disease characterized by the death of motor neurons in the spinal cord and brain. Although neurons are affected in ALS, glial cells play an important role in the disease onset and progression. Glial cells contribute to the maintenance of extracellular K+ homeostasis through the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in astrocytes and oligodendrocytes. Previous studies demonstrated impaired expression and function of Kir4.1 in astrocytes in ALS. Therefore, we first examined the role of Kir4.1 in spinal cord oligodendrocytes of the hSOD1G93A rat model by employing immunofluorescence, confocal microscopy, Western blot, and patch-clamp. We show reduced expression of Kir4.1 in oligodendrocytes in the ALS spinal cord as well as in its myelin fraction. Oligodendrocytes in culture display impaired membrane biophysical properties and decreased Kir currents, indicating their compromised functional properties. Although the expression of Kir4.1 was diminished in ALS, we observed isolated regions retaining Kir4.1 immunoreactivity in ventral horns of the hSOD1G93A spinal cord that contained cell clusters enriched in microglia. Our data show that Kir4.1+ clusters of microglia overlap with regions of pronounced presence of protein aggregates of mutated superoxide dismutase 1 that represent the hallmark of ALS. Membrane biophysical properties and Kir channel activity were not altered in neonatal ALS microglia while adult ALS microglia in culture displayed reduced Kir currents. Changes in the expression and function of Kir4.1 highlight the importance of this potassium channel in neurodegeneration suggesting Kir4.1 as a potential therapeutic target in ALS pathology.",
publisher = "Univerzitet u Beogradu, Biološki fakultet",
title = "Neurodegenerativne promene u ćelijama glije, oligodendrocitima i mikrogliji, u kičmenoj moždini na pacovskom hsod1g93a modelu amiotrofične lateralne skleroze, Neurodegenerative changes in glial cells, oligodendrocytes and microglia in the spinal cord of hsod1g93a rat model of amyotrophic lateral sclerosis",
url = "https://hdl.handle.net/21.15107/rcub_nardus_20773"
}

Perić, M.. (2022). Neurodegenerativne promene u ćelijama glije, oligodendrocitima i mikrogliji, u kičmenoj moždini na pacovskom hsod1g93a modelu amiotrofične lateralne skleroze. 
Univerzitet u Beogradu, Biološki fakultet..
https://hdl.handle.net/21.15107/rcub_nardus_20773

Perić M. Neurodegenerativne promene u ćelijama glije, oligodendrocitima i mikrogliji, u kičmenoj moždini na pacovskom hsod1g93a modelu amiotrofične lateralne skleroze. 2022;.
https://hdl.handle.net/21.15107/rcub_nardus_20773 .

Perić, Mina, "Neurodegenerativne promene u ćelijama glije, oligodendrocitima i mikrogliji, u kičmenoj moždini na pacovskom hsod1g93a modelu amiotrofične lateralne skleroze" (2022),
https://hdl.handle.net/21.15107/rcub_nardus_20773 .

TY  - CONF
AU  - Radmilović, Mihajlo
AU  - Drvenica, Ivana
AU  - Rabasović, Mihailo
AU  - Ilić, Vesna
AU  - Pavlović, Danica
AU  - Oasa, Sho
AU  - Vukojević, Vladana
AU  - Perić, Mina
AU  - Krmpot, Aleksandar
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1730
AB  - Oslikavanje eritrocita bez obeležavanja pomoću konfokalne ili
epifluorescentne mikroskopije je praktično nemoguće jer se fluorescencija od
hemoglobina (Hb) ne može detektovati zbog brzih neradijativnih raspada koji su
dominantni u odnosu na spontanu emisiju. Sa druge strane, demonstrirana je
značajna dvofotonska apsorptivnost Hb u infracrvenoj oblasti1 kao i
dvofotonski pobuđena fluorescencija (TPEF) od novoformiranog fotoprodukta2
nakon interakcije ultrakratkih laserskih impulsa sa Hb. TPEF mikroskopija je
korišćena u brojnim studijama za oslikavanje Hb i eritrocita bez obeležavanja.3
U ovom radu prikazane su fotofizičke osobine i potencijalne primene
novoformiranog fotoprodukta. Kreirane su fluorescentne mikrostrukture
pomoću direktnog laserskog upisivanja na tankim Hb slojevima (micropatterning).
Fotoprodukt je okarakterisan pomoću različitih (mikro)spektroskopskih
tehnika: emisije nakon dvofotonske apsorpcije, UV-VIS apsorpcije i spektralnog
oslikavanja. Razmatrane su spektroskopske osobine protoporfirina IX (PpIX)
pošto je on strukturni deo Hb i potencijalno može biti prekursor za formiranje
fotoprodukta. Takođe, Hb je tretiran vodonik peroksidom da bi se uočila
optička i spektroskopska sličnost tako dobijenog jedinjenja i fotoprodukta.
Potvrđena je dugovremena fotostabilnost fotoprodukta u periodima od nekoliko
meseci. Na osnovu toga što je fotoprodukt moguće dobiti na prostorno i
vremenski kontrolisan način, izvršeno je fotoobeležavanje i praćenje kretanja
pojedinačnih eritrocita u humanoj punoj krvi zdravog donora.
AB  - Осликавање еритроцита без обележавања помоћу конфокалне или
епифлуоресцентне микроскопије је практично немогуће јер се флуоресценција од
хемоглобина (Хб) не може детектовати због брзих нерадијативних распада који су
доминантни у односу на спонтану емисију. Са друге стране, демонстрирана је
значајна двофотонска апсорптивност Хб у инфрацрвеној области1 као и
двофотонски побуђена флуоресценција (ТPEF) од новоформираног фотопродукта2
након интеракције ултракратких ласерских импулса са Хб. ТPEF микроскопија је
коришћена у бројним студијама за осликавање Хб и еритроцита без обележавања.3
У овом раду приказане су фотофизичке особине и потенцијалне примене
новоформираног фотопродукта. Креиране су флуоресцентне микроструктуре
помоћу директног ласерског уписивања на танким Хб слојевима (micropatterning).
Фотопродукт је окарактерисан помоћу различитих (микро)спектроскопских
техника: емисије након двофотонске апсорпције, UV-VIS апсорпције и спектралног
осликавања. Разматране су спектроскопске особине протопорфирина IX (PpIX)
пошто је он структурни део Хб и потенцијално може бити прекурсор за формирање
фотопродукта. Такође, Хб је третиран водоник пероксидом да би се уочила
оптичка и спектроскопска сличност тако добијеног једињења и фотопродукта.
Потврђена је дуговремена фотостабилност фотопродукта у периодима од неколико
месеци. На основу тога што је фотопродукт могуће добити на просторно и
временски контролисан начин, извршено је фотообележавање и праћење кретања
појединачних еритроцита у хуманој пуној крви здравог донора.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Nelinearna laserska skenirajuća mikroskopija hemoglobina i eritrocita
T1  - Нелинеарна ласерска скенирајућа микроскопија хемоглобина и еритроцита
SP  - 19
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1730
ER  - 

@conference{
author = "Radmilović, Mihajlo and Drvenica, Ivana and Rabasović, Mihailo and Ilić, Vesna and Pavlović, Danica and Oasa, Sho and Vukojević, Vladana and Perić, Mina and Krmpot, Aleksandar",
year = "2022",
abstract = "Oslikavanje eritrocita bez obeležavanja pomoću konfokalne ili
epifluorescentne mikroskopije je praktično nemoguće jer se fluorescencija od
hemoglobina (Hb) ne može detektovati zbog brzih neradijativnih raspada koji su
dominantni u odnosu na spontanu emisiju. Sa druge strane, demonstrirana je
značajna dvofotonska apsorptivnost Hb u infracrvenoj oblasti1 kao i
dvofotonski pobuđena fluorescencija (TPEF) od novoformiranog fotoprodukta2
nakon interakcije ultrakratkih laserskih impulsa sa Hb. TPEF mikroskopija je
korišćena u brojnim studijama za oslikavanje Hb i eritrocita bez obeležavanja.3
U ovom radu prikazane su fotofizičke osobine i potencijalne primene
novoformiranog fotoprodukta. Kreirane su fluorescentne mikrostrukture
pomoću direktnog laserskog upisivanja na tankim Hb slojevima (micropatterning).
Fotoprodukt je okarakterisan pomoću različitih (mikro)spektroskopskih
tehnika: emisije nakon dvofotonske apsorpcije, UV-VIS apsorpcije i spektralnog
oslikavanja. Razmatrane su spektroskopske osobine protoporfirina IX (PpIX)
pošto je on strukturni deo Hb i potencijalno može biti prekursor za formiranje
fotoprodukta. Takođe, Hb je tretiran vodonik peroksidom da bi se uočila
optička i spektroskopska sličnost tako dobijenog jedinjenja i fotoprodukta.
Potvrđena je dugovremena fotostabilnost fotoprodukta u periodima od nekoliko
meseci. Na osnovu toga što je fotoprodukt moguće dobiti na prostorno i
vremenski kontrolisan način, izvršeno je fotoobeležavanje i praćenje kretanja
pojedinačnih eritrocita u humanoj punoj krvi zdravog donora., Осликавање еритроцита без обележавања помоћу конфокалне или
епифлуоресцентне микроскопије је практично немогуће јер се флуоресценција од
хемоглобина (Хб) не може детектовати због брзих нерадијативних распада који су
доминантни у односу на спонтану емисију. Са друге стране, демонстрирана је
значајна двофотонска апсорптивност Хб у инфрацрвеној области1 као и
двофотонски побуђена флуоресценција (ТPEF) од новоформираног фотопродукта2
након интеракције ултракратких ласерских импулса са Хб. ТPEF микроскопија је
коришћена у бројним студијама за осликавање Хб и еритроцита без обележавања.3
У овом раду приказане су фотофизичке особине и потенцијалне примене
новоформираног фотопродукта. Креиране су флуоресцентне микроструктуре
помоћу директног ласерског уписивања на танким Хб слојевима (micropatterning).
Фотопродукт је окарактерисан помоћу различитих (микро)спектроскопских
техника: емисије након двофотонске апсорпције, UV-VIS апсорпције и спектралног
осликавања. Разматране су спектроскопске особине протопорфирина IX (PpIX)
пошто је он структурни део Хб и потенцијално може бити прекурсор за формирање
фотопродукта. Такође, Хб је третиран водоник пероксидом да би се уочила
оптичка и спектроскопска сличност тако добијеног једињења и фотопродукта.
Потврђена је дуговремена фотостабилност фотопродукта у периодима од неколико
месеци. На основу тога што је фотопродукт могуће добити на просторно и
временски контролисан начин, извршено је фотообележавање и праћење кретања
појединачних еритроцита у хуманој пуној крви здравог донора.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Nelinearna laserska skenirajuća mikroskopija hemoglobina i eritrocita, Нелинеарна ласерска скенирајућа микроскопија хемоглобина и еритроцита",
pages = "19",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1730"
}

Radmilović, M., Drvenica, I., Rabasović, M., Ilić, V., Pavlović, D., Oasa, S., Vukojević, V., Perić, M.,& Krmpot, A.. (2022). Nelinearna laserska skenirajuća mikroskopija hemoglobina i eritrocita. in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 19.
https://hdl.handle.net/21.15107/rcub_imagine_1730

Radmilović M, Drvenica I, Rabasović M, Ilić V, Pavlović D, Oasa S, Vukojević V, Perić M, Krmpot A. Nelinearna laserska skenirajuća mikroskopija hemoglobina i eritrocita. in Treći kongres biologa Srbije. 2022;:19.
https://hdl.handle.net/21.15107/rcub_imagine_1730 .

Radmilović, Mihajlo, Drvenica, Ivana, Rabasović, Mihailo, Ilić, Vesna, Pavlović, Danica, Oasa, Sho, Vukojević, Vladana, Perić, Mina, Krmpot, Aleksandar, "Nelinearna laserska skenirajuća mikroskopija hemoglobina i eritrocita" in Treći kongres biologa Srbije (2022):19,
https://hdl.handle.net/21.15107/rcub_imagine_1730 .

TY  - JOUR
AU  - Lazić, Andrijana
AU  - Balint, Vanda
AU  - Stanisavljević Ninković, Danijela
AU  - Perić, Mina
AU  - Stevanović, Milena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1602
AB  - Astrocytes, as the most abundant glial cells in the central nervous system, are tightly integrated into neural networks and participate in numerous aspects of brain physiology and pathology. They are the main homeostatic cells in the central nervous system, and the loss of astrocyte physiological functions and/or gain of pro-inflammatory functions, due to their reactivation or cellular senescence, can have profound impacts on the surrounding microenvironment with pathological outcomes. Although the importance of astrocytes is generally recognized, and both senescence and reactive astrogliosis have been extensively reviewed independently, there are only a few comparative overviews of these complex processes. In this review, we summarize the latest data regarding astrocyte reactivation and senescence, and outline similarities and differences between these phenotypes from morphological, functional, and molecular points of view. A special focus has been given to neurodegenerative diseases, where these phenotypic alternations of astrocytes are significantly implicated. We also summarize current perspectives regarding new advances in model systems based on astrocytes as well as data pointing to these glial cells as potential therapeutic targets.
PB  - MDPI, Basel
T2  - International Journal of Molecular Sciences
T1  - Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies
IS  - 9
VL  - 23
DO  - 10.3390/ijms23094995
ER  - 

@article{
author = "Lazić, Andrijana and Balint, Vanda and Stanisavljević Ninković, Danijela and Perić, Mina and Stevanović, Milena",
year = "2022",
abstract = "Astrocytes, as the most abundant glial cells in the central nervous system, are tightly integrated into neural networks and participate in numerous aspects of brain physiology and pathology. They are the main homeostatic cells in the central nervous system, and the loss of astrocyte physiological functions and/or gain of pro-inflammatory functions, due to their reactivation or cellular senescence, can have profound impacts on the surrounding microenvironment with pathological outcomes. Although the importance of astrocytes is generally recognized, and both senescence and reactive astrogliosis have been extensively reviewed independently, there are only a few comparative overviews of these complex processes. In this review, we summarize the latest data regarding astrocyte reactivation and senescence, and outline similarities and differences between these phenotypes from morphological, functional, and molecular points of view. A special focus has been given to neurodegenerative diseases, where these phenotypic alternations of astrocytes are significantly implicated. We also summarize current perspectives regarding new advances in model systems based on astrocytes as well as data pointing to these glial cells as potential therapeutic targets.",
publisher = "MDPI, Basel",
journal = "International Journal of Molecular Sciences",
title = "Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies",
number = "9",
volume = "23",
doi = "10.3390/ijms23094995"
}

Lazić, A., Balint, V., Stanisavljević Ninković, D., Perić, M.,& Stevanović, M.. (2022). Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies. in International Journal of Molecular Sciences
MDPI, Basel., 23(9).
https://doi.org/10.3390/ijms23094995

Lazić A, Balint V, Stanisavljević Ninković D, Perić M, Stevanović M. Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies. in International Journal of Molecular Sciences. 2022;23(9).
doi:10.3390/ijms23094995 .

Lazić, Andrijana, Balint, Vanda, Stanisavljević Ninković, Danijela, Perić, Mina, Stevanović, Milena, "Reactive and Senescent Astroglial Phenotypes as Hallmarks of Brain Pathologies" in International Journal of Molecular Sciences, 23, no. 9 (2022),
https://doi.org/10.3390/ijms23094995 . .

TY  - JOUR
AU  - Mandić, Marija
AU  - Mitić, Katarina
AU  - Nedeljković, Predrag
AU  - Perić, Mina
AU  - Bozić, Bojan
AU  - Lunić, Tanja
AU  - Bacić, Ana
AU  - Rajilić-Stojanović, Mirjana
AU  - Peković, Sanja
AU  - Nedeljković, Biljana Bozic
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1567
AB  - The present study aimed to investigate the neuroprotective effects of the vitamin B complex (B1, B2, B3, B5, B6, and B12-VBC), by studying the changes in the femoral nerve, quadriceps muscle, popliteal lymph nodes and gut microbiota in the rat model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). VBC treatment attenuated clinical signs of EAE during the disease, and reduced the duration of EAE thereby contributing to a faster recovery. In VBC-treated EAE rats, a significant decrease in nerve and muscle nuclear density was revealed during the onset period of the disease, while a marked increase was detected at the end of the disease, compared with untreated EAE rats. In the lymph nodes of VBC-treated EAE rats, a fewer number of lymphoid follicles in the cortical area and smaller epithelioid granulomas were detected. The changes in microbiota composition were examined using 16S rRNA gene sequencing and bioinformatics analysis, which revealed the potential of VBC treatment in establishing and/or maintaining gut microbiota homeostasis. Finally, the present study demonstrated that VBC treatment ameliorated the cellular changes in the affected peripheral nerve, muscles innervated by this nerve, and the gut microbiota dysbiosis which occurred during the EAE.
PB  - MDPI, Basel
T2  - Nutrients
T1  - Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis
IS  - 6
VL  - 14
DO  - 10.3390/nu14061273
ER  - 

@article{
author = "Mandić, Marija and Mitić, Katarina and Nedeljković, Predrag and Perić, Mina and Bozić, Bojan and Lunić, Tanja and Bacić, Ana and Rajilić-Stojanović, Mirjana and Peković, Sanja and Nedeljković, Biljana Bozic",
year = "2022",
abstract = "The present study aimed to investigate the neuroprotective effects of the vitamin B complex (B1, B2, B3, B5, B6, and B12-VBC), by studying the changes in the femoral nerve, quadriceps muscle, popliteal lymph nodes and gut microbiota in the rat model of multiple sclerosis, experimental autoimmune encephalomyelitis (EAE). VBC treatment attenuated clinical signs of EAE during the disease, and reduced the duration of EAE thereby contributing to a faster recovery. In VBC-treated EAE rats, a significant decrease in nerve and muscle nuclear density was revealed during the onset period of the disease, while a marked increase was detected at the end of the disease, compared with untreated EAE rats. In the lymph nodes of VBC-treated EAE rats, a fewer number of lymphoid follicles in the cortical area and smaller epithelioid granulomas were detected. The changes in microbiota composition were examined using 16S rRNA gene sequencing and bioinformatics analysis, which revealed the potential of VBC treatment in establishing and/or maintaining gut microbiota homeostasis. Finally, the present study demonstrated that VBC treatment ameliorated the cellular changes in the affected peripheral nerve, muscles innervated by this nerve, and the gut microbiota dysbiosis which occurred during the EAE.",
publisher = "MDPI, Basel",
journal = "Nutrients",
title = "Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis",
number = "6",
volume = "14",
doi = "10.3390/nu14061273"
}

Mandić, M., Mitić, K., Nedeljković, P., Perić, M., Bozić, B., Lunić, T., Bacić, A., Rajilić-Stojanović, M., Peković, S.,& Nedeljković, B. B.. (2022). Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis. in Nutrients
MDPI, Basel., 14(6).
https://doi.org/10.3390/nu14061273

Mandić M, Mitić K, Nedeljković P, Perić M, Bozić B, Lunić T, Bacić A, Rajilić-Stojanović M, Peković S, Nedeljković BB. Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis. in Nutrients. 2022;14(6).
doi:10.3390/nu14061273 .

Mandić, Marija, Mitić, Katarina, Nedeljković, Predrag, Perić, Mina, Bozić, Bojan, Lunić, Tanja, Bacić, Ana, Rajilić-Stojanović, Mirjana, Peković, Sanja, Nedeljković, Biljana Bozic, "Vitamin B Complex and Experimental Autoimmune Encephalomyelitis -Attenuation of the Clinical Signs and Gut Microbiota Dysbiosis" in Nutrients, 14, no. 6 (2022),
https://doi.org/10.3390/nu14061273 . .

TY  - JOUR
AU  - Pislar, Anja
AU  - Nedeljković, Biljana Bozic
AU  - Perić, Mina
AU  - Jakos, Tanja
AU  - Zidar, Nace
AU  - Kos, Janko
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1535
AB  - Microglia are resident macrophages in the central nervous system that are involved in immune responses driven by Toll-like receptors (TLRs). Microglia-mediated inflammation can lead to central nervous system disorders, and more than one TLR might be involved in these pathological processes. The cysteine peptidase cathepsin X has been recognized as a pathogenic factor for inflammation-induced neurodegeneration. Here, we hypothesized that simultaneous TLR3 and TLR4 activation induces synergized microglia responses and that these phenotype changes affect cathepsin X expression and activity. Murine microglia BV2 cells and primary murine microglia were exposed to the TLR3 ligand polyinosinic-polycytidylic acid (poly(I:C)) and the TLR4 ligand lipopolysaccharide (LPS), individually and simultaneously. TLR3 and TLR4 co-activation resulted in increased inflammatory responses compared to individual TLR activation, where poly(I:C) and LPS induced distinct patterns of proinflammatory factors together with different patterns of cathepsin X expression and activity. TLR co-activation decreased intracellular cathepsin X activity and increased cathepsin X localization at the plasma membrane with concomitant increased extracellular cathepsin X protein levels and activity. Inhibition of cathepsin X in BV2 cells by AMS36, cathepsin X inhibitor, significantly reduced the poly(I:C)- and LPS-induced production of proinflammatory cytokines as well as apoptosis. Additionally, inhibiting the TLR3 and TLR4 common signaling pathway, PI3K, with LY294002 reduced the inflammatory responses of the poly(I:C)- and LPS-activated microglia and recovered cathepsin X activity. We here provide evidence that microglial cathepsin X strengthens microglia activation and leads to subsequent inflammation-induced neurodegeneration. As such, cathepsin X represents a therapeutic target for treating neurodegenerative diseases related to excess inflammation.
PB  - Springer, New York
T2  - Molecular Neurobiology
T1  - Cysteine Peptidase Cathepsin X as a Therapeutic Target for Simultaneous TLR3/4-mediated Microglia Activation
EP  - 2276
IS  - 4
SP  - 2258
VL  - 59
DO  - 10.1007/s12035-021-02694-2
ER  - 

@article{
author = "Pislar, Anja and Nedeljković, Biljana Bozic and Perić, Mina and Jakos, Tanja and Zidar, Nace and Kos, Janko",
year = "2022",
abstract = "Microglia are resident macrophages in the central nervous system that are involved in immune responses driven by Toll-like receptors (TLRs). Microglia-mediated inflammation can lead to central nervous system disorders, and more than one TLR might be involved in these pathological processes. The cysteine peptidase cathepsin X has been recognized as a pathogenic factor for inflammation-induced neurodegeneration. Here, we hypothesized that simultaneous TLR3 and TLR4 activation induces synergized microglia responses and that these phenotype changes affect cathepsin X expression and activity. Murine microglia BV2 cells and primary murine microglia were exposed to the TLR3 ligand polyinosinic-polycytidylic acid (poly(I:C)) and the TLR4 ligand lipopolysaccharide (LPS), individually and simultaneously. TLR3 and TLR4 co-activation resulted in increased inflammatory responses compared to individual TLR activation, where poly(I:C) and LPS induced distinct patterns of proinflammatory factors together with different patterns of cathepsin X expression and activity. TLR co-activation decreased intracellular cathepsin X activity and increased cathepsin X localization at the plasma membrane with concomitant increased extracellular cathepsin X protein levels and activity. Inhibition of cathepsin X in BV2 cells by AMS36, cathepsin X inhibitor, significantly reduced the poly(I:C)- and LPS-induced production of proinflammatory cytokines as well as apoptosis. Additionally, inhibiting the TLR3 and TLR4 common signaling pathway, PI3K, with LY294002 reduced the inflammatory responses of the poly(I:C)- and LPS-activated microglia and recovered cathepsin X activity. We here provide evidence that microglial cathepsin X strengthens microglia activation and leads to subsequent inflammation-induced neurodegeneration. As such, cathepsin X represents a therapeutic target for treating neurodegenerative diseases related to excess inflammation.",
publisher = "Springer, New York",
journal = "Molecular Neurobiology",
title = "Cysteine Peptidase Cathepsin X as a Therapeutic Target for Simultaneous TLR3/4-mediated Microglia Activation",
pages = "2276-2258",
number = "4",
volume = "59",
doi = "10.1007/s12035-021-02694-2"
}

Pislar, A., Nedeljković, B. B., Perić, M., Jakos, T., Zidar, N.,& Kos, J.. (2022). Cysteine Peptidase Cathepsin X as a Therapeutic Target for Simultaneous TLR3/4-mediated Microglia Activation. in Molecular Neurobiology
Springer, New York., 59(4), 2258-2276.
https://doi.org/10.1007/s12035-021-02694-2

Pislar A, Nedeljković BB, Perić M, Jakos T, Zidar N, Kos J. Cysteine Peptidase Cathepsin X as a Therapeutic Target for Simultaneous TLR3/4-mediated Microglia Activation. in Molecular Neurobiology. 2022;59(4):2258-2276.
doi:10.1007/s12035-021-02694-2 .

Pislar, Anja, Nedeljković, Biljana Bozic, Perić, Mina, Jakos, Tanja, Zidar, Nace, Kos, Janko, "Cysteine Peptidase Cathepsin X as a Therapeutic Target for Simultaneous TLR3/4-mediated Microglia Activation" in Molecular Neurobiology, 59, no. 4 (2022):2258-2276,
https://doi.org/10.1007/s12035-021-02694-2 . .

TY  - JOUR
AU  - Bijelić, Dunja
AU  - Adžić, Marija
AU  - Perić, Mina
AU  - Reiss, Gebhard
AU  - Milosević, Milena
AU  - Andjus, Pavle R.
AU  - Jakovcevski, Igor
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1522
AB  - Understanding processes that occur after injuries to the central nervous system is essential in order to gain insight into how the restoration of function can be improved. Extracellular glycoprotein tenascin-C (TnC) has numerous functions in wound healing process depending on the expression time, location, isoform and binding partners which makes it interesting to study in this context. We used an in vitro injury model, the mixed culture of cortical astrocytes and microglia, and observed that without TnC microglial cells tend to populate gap area in greater numbers and proliferate more, whereas astrocytes build up in the border region to promote faster gap closure. Alternatively spliced domain of TnC, fibronectin type III-like repeat D (FnD) strongly affected physiological properties and morphology of both astrocytes and microglia in this injury model. The rate of microglial proliferation in the injury region decreased significantly with the addition of FnD. Additionally, density of microglia also decreased, in part due to reduced proliferation, and possibly due to reduced migration and increased contact inhibition between enlarged FnD-treated cells. Overall morphology of FnD-treated microglia resembled the activated pro-inflammatory cells, and elevated expression of iNOS was in accordance with this phenotype. The effect of FnD on astrocytes was different, as it did not affect their proliferation, but stimulated migration of reactivated astrocytes into the scratched area 48 h after the lesion. Elevated expression and secretion of TNF-alpha and IL-1 beta upon FnD treatment indicated the onset of inflammation. Furthermore, on Western blots we observed increased intensity of precursor bands of beta 1 integrin and appearance of monomeric bands of P2Y12R after FnD treatment which substantiates and clarifies its role in cellular shape and motility changes. Our results show versatile functions of TnC and in particular FnD after injury, mostly contributing to ongoing inflammation in the injury region. Based on our findings, FnD might be instrumental in limiting immune cell infiltration, and promoting astrocyte migration within the injury region, thus influencing spaciotemporal organization of the wound and surrounding area.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Cell and Developmental Biology
T1  - Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injury in vitro
VL  - 10
DO  - 10.3389/fcell.2022.952208
ER  - 

@article{
author = "Bijelić, Dunja and Adžić, Marija and Perić, Mina and Reiss, Gebhard and Milosević, Milena and Andjus, Pavle R. and Jakovcevski, Igor",
year = "2022",
abstract = "Understanding processes that occur after injuries to the central nervous system is essential in order to gain insight into how the restoration of function can be improved. Extracellular glycoprotein tenascin-C (TnC) has numerous functions in wound healing process depending on the expression time, location, isoform and binding partners which makes it interesting to study in this context. We used an in vitro injury model, the mixed culture of cortical astrocytes and microglia, and observed that without TnC microglial cells tend to populate gap area in greater numbers and proliferate more, whereas astrocytes build up in the border region to promote faster gap closure. Alternatively spliced domain of TnC, fibronectin type III-like repeat D (FnD) strongly affected physiological properties and morphology of both astrocytes and microglia in this injury model. The rate of microglial proliferation in the injury region decreased significantly with the addition of FnD. Additionally, density of microglia also decreased, in part due to reduced proliferation, and possibly due to reduced migration and increased contact inhibition between enlarged FnD-treated cells. Overall morphology of FnD-treated microglia resembled the activated pro-inflammatory cells, and elevated expression of iNOS was in accordance with this phenotype. The effect of FnD on astrocytes was different, as it did not affect their proliferation, but stimulated migration of reactivated astrocytes into the scratched area 48 h after the lesion. Elevated expression and secretion of TNF-alpha and IL-1 beta upon FnD treatment indicated the onset of inflammation. Furthermore, on Western blots we observed increased intensity of precursor bands of beta 1 integrin and appearance of monomeric bands of P2Y12R after FnD treatment which substantiates and clarifies its role in cellular shape and motility changes. Our results show versatile functions of TnC and in particular FnD after injury, mostly contributing to ongoing inflammation in the injury region. Based on our findings, FnD might be instrumental in limiting immune cell infiltration, and promoting astrocyte migration within the injury region, thus influencing spaciotemporal organization of the wound and surrounding area.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Cell and Developmental Biology",
title = "Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injury in vitro",
volume = "10",
doi = "10.3389/fcell.2022.952208"
}

Bijelić, D., Adžić, M., Perić, M., Reiss, G., Milosević, M., Andjus, P. R.,& Jakovcevski, I.. (2022). Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injury in vitro. in Frontiers in Cell and Developmental Biology
Frontiers Media Sa, Lausanne., 10.
https://doi.org/10.3389/fcell.2022.952208

Bijelić D, Adžić M, Perić M, Reiss G, Milosević M, Andjus PR, Jakovcevski I. Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injury in vitro. in Frontiers in Cell and Developmental Biology. 2022;10.
doi:10.3389/fcell.2022.952208 .

Bijelić, Dunja, Adžić, Marija, Perić, Mina, Reiss, Gebhard, Milosević, Milena, Andjus, Pavle R., Jakovcevski, Igor, "Tenascin-C fibronectin D domain is involved in the fine-tuning of glial response to CNS injury in vitro" in Frontiers in Cell and Developmental Biology, 10 (2022),
https://doi.org/10.3389/fcell.2022.952208 . .

TY  - JOUR
AU  - Perić, Mina
AU  - Bataveljić, Danijela
AU  - Bijelić, Dunja
AU  - Milicević, Katarina
AU  - Andjus, Pavle R.
AU  - Pristov, Jelena Bogdanovic
AU  - Nikolić, Ljiljana
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1531
AB  - We describe an approach for studying the physiology of single live cells using the conceptionally novel upright microscope/patch-clamp configuration. Electrophysiology experiments typically require a microscope with the fixed stage position and the motion control of the microscope objective. Here, we demonstrate that a microscope with a z-axis movable stage and a fixed objective can also be efficiently used in combination with the patch-clamp technique. We define a set of underlying principles governing the operation of this microscope/patch-clamp configuration and demonstrate its performance in practice using cultured astrocytes, microglia, and oligodendrocytes. Experimental results show that our custom configuration provides stable recordings, has a high success rate of the whole-cell patch-clamp trials, can be effectively applied to study cellular physiology of glial cells, and provides comparable performance and usability to the commercially available systems. Our system can be easily replicated or adapted to suit the needs of the research groups and can be cost-effective in reducing the investments in purchasing additional equipment. We provide step-by-step instructions on implementing an upright microscope with z-axis movable stage as a routine workhorse for patch-clamping.
PB  - Wiley, Hoboken
T2  - Microscopy Research and Technique
T1  - Approach for patch-clamping using an upright microscope with z-axis movable stage
EP  - 2104
IS  - 6
SP  - 2095
VL  - 85
DO  - 10.1002/jemt.24066
ER  - 

@article{
author = "Perić, Mina and Bataveljić, Danijela and Bijelić, Dunja and Milicević, Katarina and Andjus, Pavle R. and Pristov, Jelena Bogdanovic and Nikolić, Ljiljana",
year = "2022",
abstract = "We describe an approach for studying the physiology of single live cells using the conceptionally novel upright microscope/patch-clamp configuration. Electrophysiology experiments typically require a microscope with the fixed stage position and the motion control of the microscope objective. Here, we demonstrate that a microscope with a z-axis movable stage and a fixed objective can also be efficiently used in combination with the patch-clamp technique. We define a set of underlying principles governing the operation of this microscope/patch-clamp configuration and demonstrate its performance in practice using cultured astrocytes, microglia, and oligodendrocytes. Experimental results show that our custom configuration provides stable recordings, has a high success rate of the whole-cell patch-clamp trials, can be effectively applied to study cellular physiology of glial cells, and provides comparable performance and usability to the commercially available systems. Our system can be easily replicated or adapted to suit the needs of the research groups and can be cost-effective in reducing the investments in purchasing additional equipment. We provide step-by-step instructions on implementing an upright microscope with z-axis movable stage as a routine workhorse for patch-clamping.",
publisher = "Wiley, Hoboken",
journal = "Microscopy Research and Technique",
title = "Approach for patch-clamping using an upright microscope with z-axis movable stage",
pages = "2104-2095",
number = "6",
volume = "85",
doi = "10.1002/jemt.24066"
}

Perić, M., Bataveljić, D., Bijelić, D., Milicević, K., Andjus, P. R., Pristov, J. B.,& Nikolić, L.. (2022). Approach for patch-clamping using an upright microscope with z-axis movable stage. in Microscopy Research and Technique
Wiley, Hoboken., 85(6), 2095-2104.
https://doi.org/10.1002/jemt.24066

Perić M, Bataveljić D, Bijelić D, Milicević K, Andjus PR, Pristov JB, Nikolić L. Approach for patch-clamping using an upright microscope with z-axis movable stage. in Microscopy Research and Technique. 2022;85(6):2095-2104.
doi:10.1002/jemt.24066 .

Perić, Mina, Bataveljić, Danijela, Bijelić, Dunja, Milicević, Katarina, Andjus, Pavle R., Pristov, Jelena Bogdanovic, Nikolić, Ljiljana, "Approach for patch-clamping using an upright microscope with z-axis movable stage" in Microscopy Research and Technique, 85, no. 6 (2022):2095-2104,
https://doi.org/10.1002/jemt.24066 . .

TY  - JOUR
AU  - Bijelić, Dunja
AU  - Adžić, Marija
AU  - Perić, Mina
AU  - Jakovcevski, Igor
AU  - Foerster, Eckart
AU  - Schachner, Melitta
AU  - Andjus, Pavle R.
PY  - 2021
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1423
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Immunology
T1  - Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation (vol 11, 3944, 2021)
VL  - 12
DO  - 10.3389/fimmu.2021.672476
ER  - 

@article{
author = "Bijelić, Dunja and Adžić, Marija and Perić, Mina and Jakovcevski, Igor and Foerster, Eckart and Schachner, Melitta and Andjus, Pavle R.",
year = "2021",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Immunology",
title = "Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation (vol 11, 3944, 2021)",
volume = "12",
doi = "10.3389/fimmu.2021.672476"
}

Bijelić, D., Adžić, M., Perić, M., Jakovcevski, I., Foerster, E., Schachner, M.,& Andjus, P. R.. (2021). Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation (vol 11, 3944, 2021). in Frontiers in Immunology
Frontiers Media Sa, Lausanne., 12.
https://doi.org/10.3389/fimmu.2021.672476

Bijelić D, Adžić M, Perić M, Jakovcevski I, Foerster E, Schachner M, Andjus PR. Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation (vol 11, 3944, 2021). in Frontiers in Immunology. 2021;12.
doi:10.3389/fimmu.2021.672476 .

Bijelić, Dunja, Adžić, Marija, Perić, Mina, Jakovcevski, Igor, Foerster, Eckart, Schachner, Melitta, Andjus, Pavle R., "Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation (vol 11, 3944, 2021)" in Frontiers in Immunology, 12 (2021),
https://doi.org/10.3389/fimmu.2021.672476 . .

TY  - JOUR
AU  - Bijelić, Dunja
AU  - Adžić, Marija
AU  - Perić, Mina
AU  - Jakovcevski, Igor
AU  - Foerster, Eckart
AU  - Schachner, Melitta
AU  - Andjus, Pavle R.
PY  - 2021
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1462
AB  - Extracellular matrix glycoprotein tenascin-C (TnC) is highly expressed in vertebrates during embryonic development and thereafter transiently in tissue niches undergoing extensive remodeling during regeneration after injury. TnC's different functions can be attributed to its multimodular structure represented by distinct domains and alternatively spliced isoforms. Upon central nervous system injury, TnC is upregulated and secreted into the extracellular matrix mainly by astrocytes. The goal of the present study was to elucidate the role of different TnC domains in events that take place after spinal cord injury (SCI). Astrocyte cultures prepared from TnC-deficient (TnC-/-) and wild-type (TnC+/+) mice were scratched and treated with different recombinantly generated TnC fragments. Gap closure, cell proliferation and expression of GFAP and cytokines were determined in these cultures. Gap closure in vitro was found to be delayed by TnC fragments, an effect mainly mediated by decreasing proliferation of astrocytes. The most potent effects were observed with fragments FnD, FnA and their combination. TnC-/- astrocyte cultures exhibited higher GFAP protein and mRNA expression levels, regardless of the type of fragment used for treatment. Application of TnC fragments induced also pro-inflammatory cytokine production by astrocytes in vitro. In vivo, however, the addition of FnD or Fn(D+A) led to a difference between the two genotypes, with higher levels of GFAP expression in TnC+/+ mice. FnD treatment of injured TnC-/- mice increased the density of activated microglia/macrophages in the injury region, while overall cell proliferation in the injury site was not affected. We suggest that altogether these results may explain how the reaction of astrocytes is delayed while their localization is restricted to the border of the injury site to allow microglia/macrophages to form a lesion core during the first stages of glial scar formation, as mediated by TnC and, in particular, the alternatively spliced FnD domain.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Immunology
T1  - Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation
VL  - 11
DO  - 10.3389/fimmu.2020.624612
ER  - 

@article{
author = "Bijelić, Dunja and Adžić, Marija and Perić, Mina and Jakovcevski, Igor and Foerster, Eckart and Schachner, Melitta and Andjus, Pavle R.",
year = "2021",
abstract = "Extracellular matrix glycoprotein tenascin-C (TnC) is highly expressed in vertebrates during embryonic development and thereafter transiently in tissue niches undergoing extensive remodeling during regeneration after injury. TnC's different functions can be attributed to its multimodular structure represented by distinct domains and alternatively spliced isoforms. Upon central nervous system injury, TnC is upregulated and secreted into the extracellular matrix mainly by astrocytes. The goal of the present study was to elucidate the role of different TnC domains in events that take place after spinal cord injury (SCI). Astrocyte cultures prepared from TnC-deficient (TnC-/-) and wild-type (TnC+/+) mice were scratched and treated with different recombinantly generated TnC fragments. Gap closure, cell proliferation and expression of GFAP and cytokines were determined in these cultures. Gap closure in vitro was found to be delayed by TnC fragments, an effect mainly mediated by decreasing proliferation of astrocytes. The most potent effects were observed with fragments FnD, FnA and their combination. TnC-/- astrocyte cultures exhibited higher GFAP protein and mRNA expression levels, regardless of the type of fragment used for treatment. Application of TnC fragments induced also pro-inflammatory cytokine production by astrocytes in vitro. In vivo, however, the addition of FnD or Fn(D+A) led to a difference between the two genotypes, with higher levels of GFAP expression in TnC+/+ mice. FnD treatment of injured TnC-/- mice increased the density of activated microglia/macrophages in the injury region, while overall cell proliferation in the injury site was not affected. We suggest that altogether these results may explain how the reaction of astrocytes is delayed while their localization is restricted to the border of the injury site to allow microglia/macrophages to form a lesion core during the first stages of glial scar formation, as mediated by TnC and, in particular, the alternatively spliced FnD domain.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Immunology",
title = "Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation",
volume = "11",
doi = "10.3389/fimmu.2020.624612"
}

Bijelić, D., Adžić, M., Perić, M., Jakovcevski, I., Foerster, E., Schachner, M.,& Andjus, P. R.. (2021). Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation. in Frontiers in Immunology
Frontiers Media Sa, Lausanne., 11.
https://doi.org/10.3389/fimmu.2020.624612

Bijelić D, Adžić M, Perić M, Jakovcevski I, Foerster E, Schachner M, Andjus PR. Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation. in Frontiers in Immunology. 2021;11.
doi:10.3389/fimmu.2020.624612 .

Bijelić, Dunja, Adžić, Marija, Perić, Mina, Jakovcevski, Igor, Foerster, Eckart, Schachner, Melitta, Andjus, Pavle R., "Different Functions of Recombinantly Expressed Domains of Tenascin-C in Glial Scar Formation" in Frontiers in Immunology, 11 (2021),
https://doi.org/10.3389/fimmu.2020.624612 . .

TY  - JOUR
AU  - Perić, Mina
AU  - Nikolić, Ljiljana
AU  - Andjus, Pavle R.
AU  - Bataveljić, Danijela
PY  - 2021
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1467
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1(G93A) rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+. First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1(G93A) rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1(G93A) spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1(G93A) oligodendrocytes. In addition, the Ba2+-sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1(G93A) spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.
PB  - Wiley, Hoboken
T2  - European Journal of Neuroscience
T1  - Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis
EP  - 6354
IS  - 7
SP  - 6339
VL  - 54
DO  - 10.1111/ejn.15451
ER  - 

@article{
author = "Perić, Mina and Nikolić, Ljiljana and Andjus, Pavle R. and Bataveljić, Danijela",
year = "2021",
abstract = "Amyotrophic lateral sclerosis (ALS) is a fatal neurodegenerative disease caused by the death of motor neurons in the spinal cord and the brain. Although this disease is characterized by motoneuron degeneration, non-neuronal cells such as oligodendrocytes play an important role in the disease onset and progression. The aim of our study was to examine functional properties of oligodendrocytes in the SOD1(G93A) rat model of ALS with a particular focus on the inwardly rectifying potassium channel Kir4.1 that is abundantly expressed in these glial cells and plays a role in the regulation of extracellular K+. First, we demonstrate that the expression of Kir4.1 is diminished in the spinal cord oligodendrocytes of the SOD1(G93A) rat. Moreover, our data show an elevated number of dysmorphic oligodendrocytes in the ALS spinal cord that is indicative of a degenerative phenotype. In order to assess physiological properties of oligodendrocytes, we prepared cell cultures from the rat spinal cord. Oligodendrocytes isolated from the SOD1(G93A) spinal cord display similar ramification of the processes as the control but express a lower level of Kir4.1. We further demonstrate an impairment of oligodendrocyte functional properties in ALS. Remarkably, whole-cell patch-clamp recordings revealed compromised membrane biophysical properties and diminished inward currents in the SOD1(G93A) oligodendrocytes. In addition, the Ba2+-sensitive Kir currents were decreased in ALS oligodendrocytes. Altogether, our findings provide the evidence of impaired Kir4.1 expression and function in oligodendrocytes of the SOD1(G93A) spinal cord, suggesting oligodendrocyte Kir4.1 channel as a potential contributor to the ALS pathophysiology.",
publisher = "Wiley, Hoboken",
journal = "European Journal of Neuroscience",
title = "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis",
pages = "6354-6339",
number = "7",
volume = "54",
doi = "10.1111/ejn.15451"
}

Perić, M., Nikolić, L., Andjus, P. R.,& Bataveljić, D.. (2021). Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis. in European Journal of Neuroscience
Wiley, Hoboken., 54(7), 6339-6354.
https://doi.org/10.1111/ejn.15451

Perić M, Nikolić L, Andjus PR, Bataveljić D. Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis. in European Journal of Neuroscience. 2021;54(7):6339-6354.
doi:10.1111/ejn.15451 .

Perić, Mina, Nikolić, Ljiljana, Andjus, Pavle R., Bataveljić, Danijela, "Dysfunction of oligodendrocyte inwardly rectifying potassium channel in a rat model of amyotrophic lateral sclerosis" in European Journal of Neuroscience, 54, no. 7 (2021):6339-6354,
https://doi.org/10.1111/ejn.15451 . .

TY  - JOUR
AU  - Jara, Javier H.
AU  - Sheets, Patrick L.
AU  - Nigro, Maximiliano Jose
AU  - Perić, Mina
AU  - Brooks, Carolyn
AU  - Heller, Daniel B.
AU  - Martina, Marco
AU  - Andjus, Pavle R.
AU  - Ozdinler, P. Hande
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1327
AB  - The brain is complex and heterogeneous. Even though numerous independent studies indicate cortical hyperexcitability as a potential contributor to amyotrophic lateral sclerosis (ALS) pathology, the mechanisms that are responsible for upper motor neuron (UMN) vulnerability remain elusive. To reveal the electrophysiological determinants of corticospinal motor neuron (CSMN, a.k.a UMN in mice) vulnerability, we investigated the motor cortex of hSOD1(G93A) mice at P30 (postnatal day 30), a presymptomatic time point. Glutamate uncaging by laser scanning photostimulation (LSPS) revealed altered dynamics especially within the inhibitory circuitry and more specifically in L2/3 of the motor cortex, whereas the excitatory microcircuits were unchanged. Observed microcircuitry changes were specific to CSMN in the motor column. Electrophysiological evaluation of the intrinsic properties in response to the microcircuit changes, as well as the exon microarray expression profiles of CSMN isolated from hSOD1(G93A) and healthy mice at P30, revealed the presence of a very dynamic set of events, ultimately directed to establish, maintain and retain the balance at this early stage. Also, the expression profile of key voltage-gated potassium and sodium channel subunits as well as of the inhibitory GABA receptor subunits and modulatory proteins began to suggest the challenges CSMN face at this early age. Since neurodegeneration is initiated when neurons can no longer maintain balance, the complex cellular events that occur at this critical time point help reveal how CSMN try to cope with the challenges of disease manifestation. This information is critically important for the proper modulation of UMNs and for developing effective treatment strategies.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Molecular Neuroscience
T1  - The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS
VL  - 13
DO  - 10.3389/fnmol.2020.00073
ER  - 

@article{
author = "Jara, Javier H. and Sheets, Patrick L. and Nigro, Maximiliano Jose and Perić, Mina and Brooks, Carolyn and Heller, Daniel B. and Martina, Marco and Andjus, Pavle R. and Ozdinler, P. Hande",
year = "2020",
abstract = "The brain is complex and heterogeneous. Even though numerous independent studies indicate cortical hyperexcitability as a potential contributor to amyotrophic lateral sclerosis (ALS) pathology, the mechanisms that are responsible for upper motor neuron (UMN) vulnerability remain elusive. To reveal the electrophysiological determinants of corticospinal motor neuron (CSMN, a.k.a UMN in mice) vulnerability, we investigated the motor cortex of hSOD1(G93A) mice at P30 (postnatal day 30), a presymptomatic time point. Glutamate uncaging by laser scanning photostimulation (LSPS) revealed altered dynamics especially within the inhibitory circuitry and more specifically in L2/3 of the motor cortex, whereas the excitatory microcircuits were unchanged. Observed microcircuitry changes were specific to CSMN in the motor column. Electrophysiological evaluation of the intrinsic properties in response to the microcircuit changes, as well as the exon microarray expression profiles of CSMN isolated from hSOD1(G93A) and healthy mice at P30, revealed the presence of a very dynamic set of events, ultimately directed to establish, maintain and retain the balance at this early stage. Also, the expression profile of key voltage-gated potassium and sodium channel subunits as well as of the inhibitory GABA receptor subunits and modulatory proteins began to suggest the challenges CSMN face at this early age. Since neurodegeneration is initiated when neurons can no longer maintain balance, the complex cellular events that occur at this critical time point help reveal how CSMN try to cope with the challenges of disease manifestation. This information is critically important for the proper modulation of UMNs and for developing effective treatment strategies.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Molecular Neuroscience",
title = "The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS",
volume = "13",
doi = "10.3389/fnmol.2020.00073"
}

Jara, J. H., Sheets, P. L., Nigro, M. J., Perić, M., Brooks, C., Heller, D. B., Martina, M., Andjus, P. R.,& Ozdinler, P. H.. (2020). The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS. in Frontiers in Molecular Neuroscience
Frontiers Media Sa, Lausanne., 13.
https://doi.org/10.3389/fnmol.2020.00073

Jara JH, Sheets PL, Nigro MJ, Perić M, Brooks C, Heller DB, Martina M, Andjus PR, Ozdinler PH. The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS. in Frontiers in Molecular Neuroscience. 2020;13.
doi:10.3389/fnmol.2020.00073 .

Jara, Javier H., Sheets, Patrick L., Nigro, Maximiliano Jose, Perić, Mina, Brooks, Carolyn, Heller, Daniel B., Martina, Marco, Andjus, Pavle R., Ozdinler, P. Hande, "The Electrophysiological Determinants of Corticospinal Motor Neuron Vulnerability in ALS" in Frontiers in Molecular Neuroscience, 13 (2020),
https://doi.org/10.3389/fnmol.2020.00073 . .

TY  - JOUR
AU  - Mijailović, Iva
AU  - Nikolić, Nadja
AU  - Đinić, Ana
AU  - Carkić, Jelena
AU  - Milinković, Iva
AU  - Perić, Mina
AU  - Janković, Sasha
AU  - Milašin, Jelena
AU  - Aleksić, Zoran
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1397
AB  - Background The exact mechanisms of bone resorption in periodontitis have not been fully elucidated. The aims of this study were to analyze the expression of Notch signaling molecules, bone remodeling mediators, and pro-inflammatory cytokines in periodontitis patients and to determine their potential correlations. Methods The study included 130 individuals: 40 with aggressive periodontitis (AP group), 40 with chronic periodontitis (CP group), and 50 periodontally healthy controls. Total RNA was extracted from gingival crevicular fluid samples and relative gene expression of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG) was determined by reverse transcriptase - real-time polymerase chain reaction (RT-qPCR). Results In AP group, a significant increase of Notch 2, TNF-alpha, IL-17 and RANKL and a significant decrease of Notch 1 and Jagged 1 expression were observed compared to control group (P = 0.023, P = 0.005, P = 0.030, and P = 0.001 P = 0.031 and P = 0.029, respectively). Notch 2 and RANKL were also overexpressed in CP group compared to controls (P = 0.001 and P = 0.011). Significant correlations were observed in AP group between expression levels of the analyzed genes. Conclusion The present findings implicate Notch 2 overexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis. The down-regulation of Notch 1 and Jagged 1 and loss of their osteoprotective function might cause a more excessive osteoclast formation and contribute to greater osteolysis in aggressive periodontitis.
PB  - Wiley, Hoboken
T2  - Journal of Periodontology
T1  - The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis
EP  - 561
IS  - 4
SP  - 554
VL  - 91
DO  - 10.1002/JPER.18-0755
ER  - 

@article{
author = "Mijailović, Iva and Nikolić, Nadja and Đinić, Ana and Carkić, Jelena and Milinković, Iva and Perić, Mina and Janković, Sasha and Milašin, Jelena and Aleksić, Zoran",
year = "2020",
abstract = "Background The exact mechanisms of bone resorption in periodontitis have not been fully elucidated. The aims of this study were to analyze the expression of Notch signaling molecules, bone remodeling mediators, and pro-inflammatory cytokines in periodontitis patients and to determine their potential correlations. Methods The study included 130 individuals: 40 with aggressive periodontitis (AP group), 40 with chronic periodontitis (CP group), and 50 periodontally healthy controls. Total RNA was extracted from gingival crevicular fluid samples and relative gene expression of investigated molecules (Notch 1, Notch 2, Jagged 1, Hes 1, Hey 1, TNF-alpha, IL-17, RANKL, and OPG) was determined by reverse transcriptase - real-time polymerase chain reaction (RT-qPCR). Results In AP group, a significant increase of Notch 2, TNF-alpha, IL-17 and RANKL and a significant decrease of Notch 1 and Jagged 1 expression were observed compared to control group (P = 0.023, P = 0.005, P = 0.030, and P = 0.001 P = 0.031 and P = 0.029, respectively). Notch 2 and RANKL were also overexpressed in CP group compared to controls (P = 0.001 and P = 0.011). Significant correlations were observed in AP group between expression levels of the analyzed genes. Conclusion The present findings implicate Notch 2 overexpression in the ethiopathogenesis of bone resorption in aggressive and chronic periodontitis. The down-regulation of Notch 1 and Jagged 1 and loss of their osteoprotective function might cause a more excessive osteoclast formation and contribute to greater osteolysis in aggressive periodontitis.",
publisher = "Wiley, Hoboken",
journal = "Journal of Periodontology",
title = "The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis",
pages = "561-554",
number = "4",
volume = "91",
doi = "10.1002/JPER.18-0755"
}

Mijailović, I., Nikolić, N., Đinić, A., Carkić, J., Milinković, I., Perić, M., Janković, S., Milašin, J.,& Aleksić, Z.. (2020). The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis. in Journal of Periodontology
Wiley, Hoboken., 91(4), 554-561.
https://doi.org/10.1002/JPER.18-0755

Mijailović I, Nikolić N, Đinić A, Carkić J, Milinković I, Perić M, Janković S, Milašin J, Aleksić Z. The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis. in Journal of Periodontology. 2020;91(4):554-561.
doi:10.1002/JPER.18-0755 .

Mijailović, Iva, Nikolić, Nadja, Đinić, Ana, Carkić, Jelena, Milinković, Iva, Perić, Mina, Janković, Sasha, Milašin, Jelena, Aleksić, Zoran, "The down-regulation of Notch 1 signaling contributes to the severity of bone loss in aggressive periodontitis" in Journal of Periodontology, 91, no. 4 (2020):554-561,
https://doi.org/10.1002/JPER.18-0755 . .

TY  - JOUR
AU  - Serrano, Alessia
AU  - Apolloni, Savina
AU  - Rossi, Simona
AU  - Lattante, Serena
AU  - Sabatelli, Mario
AU  - Perić, Mina
AU  - Andjus, Pavle R.
AU  - Michetti, Fabrizio
AU  - Carri, Maria Teresa
AU  - Cozzolino, Mauro
AU  - D'Ambrosi, Nadia
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1220
AB  - S100A4, belonging to a large multifunctional S100 protein family, is a Ca2+-binding protein with a significant role in stimulating the motility of cancer and immune cells, as well as in promoting pro-inflammatory properties in different cell types. In the CNS, there is limited information concerning S100A4 presence and function. In this study, we analyzed the expression of S100A4 and the effect of the S100A4 transcriptional inhibitor niclosamide in murine activated primary microglia. We found that S100A4 was strongly up-regulated in reactive microglia and that niclosamide prevented NADPH oxidase 2, mTOR (mammalian target of rapamycin), and NF-kappa B (nuclear factor-kappa B) increase, cytoskeletal rearrangements, migration, and phagocytosis. Furthermore, we found that S100A4 was significantly up-regulated in astrocytes and microglia in the spinal cord of a transgenic rat SOD1-G93A model of amyotrophic lateral sclerosis. Finally, we demonstrated the increased expression of S100A4 also in fibroblasts derived from amyotrophic lateral sclerosis (ALS) patients carrying SOD1 pathogenic variants. These results ascribe S100A4 as a marker of microglial reactivity, suggesting the contribution of S100A4-regulated pathways to neuroinflammation, and identify niclosamide as a possible drug in the control and attenuation of reactive phenotypes of microglia, thus opening the way to further investigation for a new application in neurodegenerative conditions.
PB  - MDPI, Basel
T2  - Cells
T1  - The S100A4 Transcriptional Inhibitor Niclosamide Reduces Pro-Inflammatory and Migratory Phenotypes of Microglia: Implications for Amyotrophic Lateral Sclerosis
IS  - 10
VL  - 8
DO  - 10.3390/cells8101261
ER  - 

@article{
author = "Serrano, Alessia and Apolloni, Savina and Rossi, Simona and Lattante, Serena and Sabatelli, Mario and Perić, Mina and Andjus, Pavle R. and Michetti, Fabrizio and Carri, Maria Teresa and Cozzolino, Mauro and D'Ambrosi, Nadia",
year = "2019",
abstract = "S100A4, belonging to a large multifunctional S100 protein family, is a Ca2+-binding protein with a significant role in stimulating the motility of cancer and immune cells, as well as in promoting pro-inflammatory properties in different cell types. In the CNS, there is limited information concerning S100A4 presence and function. In this study, we analyzed the expression of S100A4 and the effect of the S100A4 transcriptional inhibitor niclosamide in murine activated primary microglia. We found that S100A4 was strongly up-regulated in reactive microglia and that niclosamide prevented NADPH oxidase 2, mTOR (mammalian target of rapamycin), and NF-kappa B (nuclear factor-kappa B) increase, cytoskeletal rearrangements, migration, and phagocytosis. Furthermore, we found that S100A4 was significantly up-regulated in astrocytes and microglia in the spinal cord of a transgenic rat SOD1-G93A model of amyotrophic lateral sclerosis. Finally, we demonstrated the increased expression of S100A4 also in fibroblasts derived from amyotrophic lateral sclerosis (ALS) patients carrying SOD1 pathogenic variants. These results ascribe S100A4 as a marker of microglial reactivity, suggesting the contribution of S100A4-regulated pathways to neuroinflammation, and identify niclosamide as a possible drug in the control and attenuation of reactive phenotypes of microglia, thus opening the way to further investigation for a new application in neurodegenerative conditions.",
publisher = "MDPI, Basel",
journal = "Cells",
title = "The S100A4 Transcriptional Inhibitor Niclosamide Reduces Pro-Inflammatory and Migratory Phenotypes of Microglia: Implications for Amyotrophic Lateral Sclerosis",
number = "10",
volume = "8",
doi = "10.3390/cells8101261"
}

Serrano, A., Apolloni, S., Rossi, S., Lattante, S., Sabatelli, M., Perić, M., Andjus, P. R., Michetti, F., Carri, M. T., Cozzolino, M.,& D'Ambrosi, N.. (2019). The S100A4 Transcriptional Inhibitor Niclosamide Reduces Pro-Inflammatory and Migratory Phenotypes of Microglia: Implications for Amyotrophic Lateral Sclerosis. in Cells
MDPI, Basel., 8(10).
https://doi.org/10.3390/cells8101261

Serrano A, Apolloni S, Rossi S, Lattante S, Sabatelli M, Perić M, Andjus PR, Michetti F, Carri MT, Cozzolino M, D'Ambrosi N. The S100A4 Transcriptional Inhibitor Niclosamide Reduces Pro-Inflammatory and Migratory Phenotypes of Microglia: Implications for Amyotrophic Lateral Sclerosis. in Cells. 2019;8(10).
doi:10.3390/cells8101261 .

Serrano, Alessia, Apolloni, Savina, Rossi, Simona, Lattante, Serena, Sabatelli, Mario, Perić, Mina, Andjus, Pavle R., Michetti, Fabrizio, Carri, Maria Teresa, Cozzolino, Mauro, D'Ambrosi, Nadia, "The S100A4 Transcriptional Inhibitor Niclosamide Reduces Pro-Inflammatory and Migratory Phenotypes of Microglia: Implications for Amyotrophic Lateral Sclerosis" in Cells, 8, no. 10 (2019),
https://doi.org/10.3390/cells8101261 . .

TY  - JOUR
AU  - Simonović, Jelena
AU  - Toljić, Bosko
AU  - Nikolić, Nadja
AU  - Perić, Mina
AU  - Vujin, Jasna
AU  - Panajotović, Radmila
AU  - Gajić, Rados
AU  - Bekyarova, Elena
AU  - Cataldi, Amelia
AU  - Parpura, Vladimir
AU  - Milašin, Jelena
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1150
AB  - Stem cell-based therapies are considered a promising treatment modality for many medical conditions. Several types of stem cells with variable differentiation potentials have been isolated from dental tissues, among them stem cells from apical papilla (SCAP). In parallel, new classes of biocompatible nanomaterials have also been developed, including graphene and carbon nanotube-based materials. The aim of the study was to assess whether graphene dispersion (GD) and water-soluble single walled carbon nanotubes (ws-SWCNT), may enhance SCAPs capacity to undergo neural differentiation. SCAPs cultivated in neuroinductive medium supplemented with GD and ws-SWCNT, separately and in combination, were subjected to neural marker analysis by real-time polymerase chain reaction (neurofilament medium [NF-M], neurogenin-2 [ngn-2], III-tubulin, microtubule-associated protein 2) and immunocytochemistry (NeuN and III-tubulin). GD, ws-SWCNT, and their combination, had neuro-stimulatory effects on SCAPs, as judged by the production of neural markers. Compared to cells grown in nanomaterial free medium, cells with GD showed higher production of B3T, cells with ws-SWCNT had higher production of ngn-2 and NF-M, while the combination of nanomaterials gave similar levels of both B3T and NF-M as the neuroinductive medium aloal ne, but with the finest neuron-like morphology. In conclusion, GD and ws-SWCNT seem to enhance neurdifferentiation of SCAP.
PB  - Wiley, Hoboken
T2  - Journal of Biomedical Materials Research Part A
T1  - Differentiation of stem cells from apical papilla into neural lineage using graphene dispersion and single walled carbon nanotubes
EP  - 2661
IS  - 10
SP  - 2653
VL  - 106
DO  - 10.1002/jbm.a.36461
ER  - 

@article{
author = "Simonović, Jelena and Toljić, Bosko and Nikolić, Nadja and Perić, Mina and Vujin, Jasna and Panajotović, Radmila and Gajić, Rados and Bekyarova, Elena and Cataldi, Amelia and Parpura, Vladimir and Milašin, Jelena",
year = "2018",
abstract = "Stem cell-based therapies are considered a promising treatment modality for many medical conditions. Several types of stem cells with variable differentiation potentials have been isolated from dental tissues, among them stem cells from apical papilla (SCAP). In parallel, new classes of biocompatible nanomaterials have also been developed, including graphene and carbon nanotube-based materials. The aim of the study was to assess whether graphene dispersion (GD) and water-soluble single walled carbon nanotubes (ws-SWCNT), may enhance SCAPs capacity to undergo neural differentiation. SCAPs cultivated in neuroinductive medium supplemented with GD and ws-SWCNT, separately and in combination, were subjected to neural marker analysis by real-time polymerase chain reaction (neurofilament medium [NF-M], neurogenin-2 [ngn-2], III-tubulin, microtubule-associated protein 2) and immunocytochemistry (NeuN and III-tubulin). GD, ws-SWCNT, and their combination, had neuro-stimulatory effects on SCAPs, as judged by the production of neural markers. Compared to cells grown in nanomaterial free medium, cells with GD showed higher production of B3T, cells with ws-SWCNT had higher production of ngn-2 and NF-M, while the combination of nanomaterials gave similar levels of both B3T and NF-M as the neuroinductive medium aloal ne, but with the finest neuron-like morphology. In conclusion, GD and ws-SWCNT seem to enhance neurdifferentiation of SCAP.",
publisher = "Wiley, Hoboken",
journal = "Journal of Biomedical Materials Research Part A",
title = "Differentiation of stem cells from apical papilla into neural lineage using graphene dispersion and single walled carbon nanotubes",
pages = "2661-2653",
number = "10",
volume = "106",
doi = "10.1002/jbm.a.36461"
}

Simonović, J., Toljić, B., Nikolić, N., Perić, M., Vujin, J., Panajotović, R., Gajić, R., Bekyarova, E., Cataldi, A., Parpura, V.,& Milašin, J.. (2018). Differentiation of stem cells from apical papilla into neural lineage using graphene dispersion and single walled carbon nanotubes. in Journal of Biomedical Materials Research Part A
Wiley, Hoboken., 106(10), 2653-2661.
https://doi.org/10.1002/jbm.a.36461

Simonović J, Toljić B, Nikolić N, Perić M, Vujin J, Panajotović R, Gajić R, Bekyarova E, Cataldi A, Parpura V, Milašin J. Differentiation of stem cells from apical papilla into neural lineage using graphene dispersion and single walled carbon nanotubes. in Journal of Biomedical Materials Research Part A. 2018;106(10):2653-2661.
doi:10.1002/jbm.a.36461 .

Simonović, Jelena, Toljić, Bosko, Nikolić, Nadja, Perić, Mina, Vujin, Jasna, Panajotović, Radmila, Gajić, Rados, Bekyarova, Elena, Cataldi, Amelia, Parpura, Vladimir, Milašin, Jelena, "Differentiation of stem cells from apical papilla into neural lineage using graphene dispersion and single walled carbon nanotubes" in Journal of Biomedical Materials Research Part A, 106, no. 10 (2018):2653-2661,
https://doi.org/10.1002/jbm.a.36461 . .

TY  - JOUR
AU  - Serrano, Alessia
AU  - Donno, Claudia
AU  - Giannetti, Stefano
AU  - Perić, Mina
AU  - Andjus, Pavle R.
AU  - D'Ambrosi, Nadia
AU  - Michetti, Fabrizio
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1074
AB  - Neuroinflammation is one of the major players in amyotrophic lateral sclerosis (ALS) pathogenesis, and astrocytes are significantly involved in this process. The astrocytic protein S100B can be released in pathological states activating the receptor for advanced glycation end products (RAGE). Different indications point to an aberrant expression of S100B and RAGE in ALS. In this work, we observed that S100B and RAGE are progressively and selectively upregulated in astrocytes of diseased rats with a tissue-specific timing pattern, correlated to the level of neurodegeneration. The expression of the full-length and soluble RAGE isoforms could also be linked to the degree of tissue damage. The mere presence of mutant SOD1 is able to increase the intracellular levels and release S100B from astrocytes, suggesting the possibility that an increased astrocytic S100B expression might be an early occurring event in the disease. Finally, our findings indicate that the protein may exert a proinflammatory role in ALS, since its inhibition in astrocytes derived from SOD1(G93A) mice limits the expression of reactivity-linked/proinflammatory genes. Thus, our results propose the S100B-RAGE axis as an effective contributor to the pathogenesis of the disease, suggesting its blockade as a rational target for a therapeutic intervention in ALS.
PB  - Hindawi Ltd, London
T2  - Mediators of Inflammation
T1  - The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes
SP  - 1626204
VL  - 2017
DO  - 10.1155/2017/1626204
ER  - 

@article{
author = "Serrano, Alessia and Donno, Claudia and Giannetti, Stefano and Perić, Mina and Andjus, Pavle R. and D'Ambrosi, Nadia and Michetti, Fabrizio",
year = "2017",
abstract = "Neuroinflammation is one of the major players in amyotrophic lateral sclerosis (ALS) pathogenesis, and astrocytes are significantly involved in this process. The astrocytic protein S100B can be released in pathological states activating the receptor for advanced glycation end products (RAGE). Different indications point to an aberrant expression of S100B and RAGE in ALS. In this work, we observed that S100B and RAGE are progressively and selectively upregulated in astrocytes of diseased rats with a tissue-specific timing pattern, correlated to the level of neurodegeneration. The expression of the full-length and soluble RAGE isoforms could also be linked to the degree of tissue damage. The mere presence of mutant SOD1 is able to increase the intracellular levels and release S100B from astrocytes, suggesting the possibility that an increased astrocytic S100B expression might be an early occurring event in the disease. Finally, our findings indicate that the protein may exert a proinflammatory role in ALS, since its inhibition in astrocytes derived from SOD1(G93A) mice limits the expression of reactivity-linked/proinflammatory genes. Thus, our results propose the S100B-RAGE axis as an effective contributor to the pathogenesis of the disease, suggesting its blockade as a rational target for a therapeutic intervention in ALS.",
publisher = "Hindawi Ltd, London",
journal = "Mediators of Inflammation",
title = "The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes",
pages = "1626204",
volume = "2017",
doi = "10.1155/2017/1626204"
}

Serrano, A., Donno, C., Giannetti, S., Perić, M., Andjus, P. R., D'Ambrosi, N.,& Michetti, F.. (2017). The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes. in Mediators of Inflammation
Hindawi Ltd, London., 2017, 1626204.
https://doi.org/10.1155/2017/1626204

Serrano A, Donno C, Giannetti S, Perić M, Andjus PR, D'Ambrosi N, Michetti F. The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes. in Mediators of Inflammation. 2017;2017:1626204.
doi:10.1155/2017/1626204 .

Serrano, Alessia, Donno, Claudia, Giannetti, Stefano, Perić, Mina, Andjus, Pavle R., D'Ambrosi, Nadia, Michetti, Fabrizio, "The Astrocytic S100B Protein with Its Receptor RAGE Is Aberrantly Expressed in SOD1(G93A) Models, and Its Inhibition Decreases the Expression of Proinflammatory Genes" in Mediators of Inflammation, 2017 (2017):1626204,
https://doi.org/10.1155/2017/1626204 . .

TY  - JOUR
AU  - Dakić, Tamara B.
AU  - Jevdjović, Tanja V.
AU  - Perić, Mina
AU  - Bjelobaba, Ivana M.
AU  - Markelić, Milica B.
AU  - Milutinović, Bojana S.
AU  - Lakić, Iva V.
AU  - Jasnić, Nebojša I.
AU  - Đorđević, Jelena
AU  - Vujović, Predrag Z.
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1094
AB  - In the hypothalamus, insulin takes on many roles involved in energy homoeostasis. Therefore, the aim of this study was to examine hypothalamic insulin expression during the initial phase of the metabolic response to fasting. Hypothalamic insulin content was assessed by both radioimmunoassay and Western blot. The relative expression of insulin mRNA was examined by qPCR. Immunofluorescence and immunohistochemistry were used to determine the distribution of insulin immunopositivity in the hypothalamus. After 6-h fasting, both glucose and insulin levels were decreased in serum but not in the cerebrospinal fluid. Our study showed for the first time that, while the concentration of circulating glucose and insulin decreased, both insulin mRNA expression and insulin content in the hypothalamic parenchyma were increased after short-term fasting. Increased insulin immunopositivity was detected specifically in the neurons of the hypothalamic periventricular nucleus and in the ependymal cells of fasting animals. These novel findings point to the complexity of mechanisms regulating insulin expression in the CNS in general and in the hypothalamus in particular.
PB  - Wiley, Hoboken
T2  - European Journal of Neuroscience
T1  - Short-term fasting promotes insulin expression in rat hypothalamus
EP  - 1737
IS  - 1
SP  - 1730
VL  - 46
DO  - 10.1111/ejn.13607
ER  - 

@article{
author = "Dakić, Tamara B. and Jevdjović, Tanja V. and Perić, Mina and Bjelobaba, Ivana M. and Markelić, Milica B. and Milutinović, Bojana S. and Lakić, Iva V. and Jasnić, Nebojša I. and Đorđević, Jelena and Vujović, Predrag Z.",
year = "2017",
abstract = "In the hypothalamus, insulin takes on many roles involved in energy homoeostasis. Therefore, the aim of this study was to examine hypothalamic insulin expression during the initial phase of the metabolic response to fasting. Hypothalamic insulin content was assessed by both radioimmunoassay and Western blot. The relative expression of insulin mRNA was examined by qPCR. Immunofluorescence and immunohistochemistry were used to determine the distribution of insulin immunopositivity in the hypothalamus. After 6-h fasting, both glucose and insulin levels were decreased in serum but not in the cerebrospinal fluid. Our study showed for the first time that, while the concentration of circulating glucose and insulin decreased, both insulin mRNA expression and insulin content in the hypothalamic parenchyma were increased after short-term fasting. Increased insulin immunopositivity was detected specifically in the neurons of the hypothalamic periventricular nucleus and in the ependymal cells of fasting animals. These novel findings point to the complexity of mechanisms regulating insulin expression in the CNS in general and in the hypothalamus in particular.",
publisher = "Wiley, Hoboken",
journal = "European Journal of Neuroscience",
title = "Short-term fasting promotes insulin expression in rat hypothalamus",
pages = "1737-1730",
number = "1",
volume = "46",
doi = "10.1111/ejn.13607"
}

Dakić, T. B., Jevdjović, T. V., Perić, M., Bjelobaba, I. M., Markelić, M. B., Milutinović, B. S., Lakić, I. V., Jasnić, N. I., Đorđević, J.,& Vujović, P. Z.. (2017). Short-term fasting promotes insulin expression in rat hypothalamus. in European Journal of Neuroscience
Wiley, Hoboken., 46(1), 1730-1737.
https://doi.org/10.1111/ejn.13607

Dakić TB, Jevdjović TV, Perić M, Bjelobaba IM, Markelić MB, Milutinović BS, Lakić IV, Jasnić NI, Đorđević J, Vujović PZ. Short-term fasting promotes insulin expression in rat hypothalamus. in European Journal of Neuroscience. 2017;46(1):1730-1737.
doi:10.1111/ejn.13607 .

Dakić, Tamara B., Jevdjović, Tanja V., Perić, Mina, Bjelobaba, Ivana M., Markelić, Milica B., Milutinović, Bojana S., Lakić, Iva V., Jasnić, Nebojša I., Đorđević, Jelena, Vujović, Predrag Z., "Short-term fasting promotes insulin expression in rat hypothalamus" in European Journal of Neuroscience, 46, no. 1 (2017):1730-1737,
https://doi.org/10.1111/ejn.13607 . .

TY  - JOUR
AU  - Perić, Mina
AU  - Mitrecić, Dinko
AU  - Andjus, Pavle R.
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1023
AB  - Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder affecting upper and lower motoneurons. The two types, sporadic and familial differ in the aetiopathogenesis but have a similar neuropathology characterized by oxidative stress, excitotoxicity and inflammation. The disease is also characterized by a non-cell autonomous mechanism with astrocytes playing a central role by affecting synaptic glutamate, the blood-brain barrier, and metabolic and trophic support. Two types of therapeutic approaches focusing on astrocytes are presented: a) emerging molecular targets (potassium inward rectifier channels and aquaporins at the astrocyte end-feet, and IP3 receptor signaling pathway), and b) cell therapy with stem cell - generated and transplanted astrocytes.
PB  - Bentham Science Publ Ltd, Sharjah
T2  - Current Pharmaceutical Design
T1  - Targeting Astrocytes for Treatment in Amyotrophic Lateral Sclerosis
EP  - 5044
IS  - 33
SP  - 5037
VL  - 23
DO  - 10.2174/1381612823666170615110446
ER  - 

@article{
author = "Perić, Mina and Mitrecić, Dinko and Andjus, Pavle R.",
year = "2017",
abstract = "Amyotrophic lateral sclerosis (ALS) is a fatal neurological disorder affecting upper and lower motoneurons. The two types, sporadic and familial differ in the aetiopathogenesis but have a similar neuropathology characterized by oxidative stress, excitotoxicity and inflammation. The disease is also characterized by a non-cell autonomous mechanism with astrocytes playing a central role by affecting synaptic glutamate, the blood-brain barrier, and metabolic and trophic support. Two types of therapeutic approaches focusing on astrocytes are presented: a) emerging molecular targets (potassium inward rectifier channels and aquaporins at the astrocyte end-feet, and IP3 receptor signaling pathway), and b) cell therapy with stem cell - generated and transplanted astrocytes.",
publisher = "Bentham Science Publ Ltd, Sharjah",
journal = "Current Pharmaceutical Design",
title = "Targeting Astrocytes for Treatment in Amyotrophic Lateral Sclerosis",
pages = "5044-5037",
number = "33",
volume = "23",
doi = "10.2174/1381612823666170615110446"
}

Perić, M., Mitrecić, D.,& Andjus, P. R.. (2017). Targeting Astrocytes for Treatment in Amyotrophic Lateral Sclerosis. in Current Pharmaceutical Design
Bentham Science Publ Ltd, Sharjah., 23(33), 5037-5044.
https://doi.org/10.2174/1381612823666170615110446

Perić M, Mitrecić D, Andjus PR. Targeting Astrocytes for Treatment in Amyotrophic Lateral Sclerosis. in Current Pharmaceutical Design. 2017;23(33):5037-5044.
doi:10.2174/1381612823666170615110446 .

Perić, Mina, Mitrecić, Dinko, Andjus, Pavle R., "Targeting Astrocytes for Treatment in Amyotrophic Lateral Sclerosis" in Current Pharmaceutical Design, 23, no. 33 (2017):5037-5044,
https://doi.org/10.2174/1381612823666170615110446 . .