TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Jovanović Stojanov, Sofija
AU  - Dragoj, Miodrag
AU  - Ljujić, Mila
PY  - 2023
UR  - https://doi.org/10.1007/s00418-022-02172-3
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2243
AB  - Identification of the signature molecular profiles involved in therapy resistance is of vital importance in developing new strategies for treatments and disease monitoring. Protein alpha-1 antitrypsin (AAT, encoded by SERPINA1 gene) is an acute-phase protein, and its high expression has been linked with unfavorable clinical outcome in different types of cancer; however, data on its involvement in therapy resistance are still insufficient. We analyzed SERPINA1 mRNA expression in three different multidrug-resistant (MDR) cell lines—U87-TxR, NCI-H460/R, and DLD1-TxR—and in U87 cells grown in alginate microfibers as a 3D cellular model of glioblastoma. Expression of IL-6 as a major modulator of SERPINA1 was also analyzed. Additionally, AAT protein expression in MDR cells was analyzed by immunofluorescence. SERPINA1 gene expression and AAT protein expression were significantly upregulated in all the tested MDR cell lines compared with their sensitive counterparts. Moreover, SERPINA1 was significantly upregulated in 3D models of glioblastoma, previously found to have upregulated drug-resistance-related gene expression compared with 2D cells. With the exception of NCI-H460/R, in all cell lines as well as in a 3D model of U87 cells, increase in SERPINA1 expression correlated with the increase in IL-6 expression. Our results indicate that AAT could be utilized as a biomarker of therapy resistance in cancer; however, further studies are needed to elucidate the mechanisms driving AAT upregulation in therapy resistance and its biological significance in this process.
T2  - Histochemistry and Cell Biology
T1  - Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells
EP  - 437
IS  - 5
SP  - 431
VL  - 159
DO  - 10.1007/s00418-022-02172-3
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Jovanović Stojanov, Sofija and Dragoj, Miodrag and Ljujić, Mila",
year = "2023",
abstract = "Identification of the signature molecular profiles involved in therapy resistance is of vital importance in developing new strategies for treatments and disease monitoring. Protein alpha-1 antitrypsin (AAT, encoded by SERPINA1 gene) is an acute-phase protein, and its high expression has been linked with unfavorable clinical outcome in different types of cancer; however, data on its involvement in therapy resistance are still insufficient. We analyzed SERPINA1 mRNA expression in three different multidrug-resistant (MDR) cell lines—U87-TxR, NCI-H460/R, and DLD1-TxR—and in U87 cells grown in alginate microfibers as a 3D cellular model of glioblastoma. Expression of IL-6 as a major modulator of SERPINA1 was also analyzed. Additionally, AAT protein expression in MDR cells was analyzed by immunofluorescence. SERPINA1 gene expression and AAT protein expression were significantly upregulated in all the tested MDR cell lines compared with their sensitive counterparts. Moreover, SERPINA1 was significantly upregulated in 3D models of glioblastoma, previously found to have upregulated drug-resistance-related gene expression compared with 2D cells. With the exception of NCI-H460/R, in all cell lines as well as in a 3D model of U87 cells, increase in SERPINA1 expression correlated with the increase in IL-6 expression. Our results indicate that AAT could be utilized as a biomarker of therapy resistance in cancer; however, further studies are needed to elucidate the mechanisms driving AAT upregulation in therapy resistance and its biological significance in this process.",
journal = "Histochemistry and Cell Biology",
title = "Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells",
pages = "437-431",
number = "5",
volume = "159",
doi = "10.1007/s00418-022-02172-3"
}

Divac Rankov, A., Jovanović Stojanov, S., Dragoj, M.,& Ljujić, M.. (2023). Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells. in Histochemistry and Cell Biology, 159(5), 431-437.
https://doi.org/10.1007/s00418-022-02172-3

Divac Rankov A, Jovanović Stojanov S, Dragoj M, Ljujić M. Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells. in Histochemistry and Cell Biology. 2023;159(5):431-437.
doi:10.1007/s00418-022-02172-3 .

Divac Rankov, Aleksandra, Jovanović Stojanov, Sofija, Dragoj, Miodrag, Ljujić, Mila, "Alpha-1 antitrypsin expression is upregulated in multidrug-resistant cancer cells" in Histochemistry and Cell Biology, 159, no. 5 (2023):431-437,
https://doi.org/10.1007/s00418-022-02172-3 . .

TY  - CONF
AU  - Ljujić, Mila
AU  - Trifunović, Sara
AU  - Ilić, Bojan
AU  - Milovanović, Jelena
AU  - Dinić, Jelena
AU  - Divac Rankov, Aleksandra
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2130
AB  - Introduction: Cigarette smoke exposure is a known risk factor for development of lung diseases and
electronic cigarettes(e-cigarettes) were introduced as a popular and safer alternative to combustible tobacco products. Increasing number of studies are reporting their adverse biological effects both in vivo
and in vitro. Aim of this study was to evaluate the effect of e-cigarettes on mitochondrial function in
lung bronchial epithelial cells.
Methods: Electronic cigarette vapor condensate (ECC) was generated using an e-cigarette device on a
suction trap cooled in a dry ice/ethanol bath.We used unflavoured and flavoured e-cigarette liquids with
and without nicotine. Human bronchial epithelial BEAS2B cells were seeded in 96well plates and treated
with 2% e-cigarette vapour condensate for 24h. Mitochondrial membrane potential was measured using
50nM TMRE (Tetramethyl rhodamine ethyl ester) and cells were visualized on ImageXpress® Pico Automated Cell Imaging System (Molecular Devices, San Jose, CA, USA) with a 10x objective.
Results: We found a significant reduction of TMRE fluorescence in treated cells compared to the control. Imaging of treated cells also revealed changes in cell morphology and the presence of mitochondria in TNT-like structures.
Conclusion: Mitochondrial dysfunction has been associated with various pathological conditions including lung diseases such as asthma, COPD and lung cancer. Due to their relative novelty, the role of
electronic cigarette use in development of chronic lung diseasesisstill relatively unknown. Our findings
contribute to the growing list of studies pointing to their adverse biological effects and imply their involvement in processes contributing to chronic lung diseases.
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  - Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell
EP  - 139
SP  - 139
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2130
ER  - 

@conference{
author = "Ljujić, Mila and Trifunović, Sara and Ilić, Bojan and Milovanović, Jelena and Dinić, Jelena and Divac Rankov, Aleksandra",
year = "2023",
abstract = "Introduction: Cigarette smoke exposure is a known risk factor for development of lung diseases and
electronic cigarettes(e-cigarettes) were introduced as a popular and safer alternative to combustible tobacco products. Increasing number of studies are reporting their adverse biological effects both in vivo
and in vitro. Aim of this study was to evaluate the effect of e-cigarettes on mitochondrial function in
lung bronchial epithelial cells.
Methods: Electronic cigarette vapor condensate (ECC) was generated using an e-cigarette device on a
suction trap cooled in a dry ice/ethanol bath.We used unflavoured and flavoured e-cigarette liquids with
and without nicotine. Human bronchial epithelial BEAS2B cells were seeded in 96well plates and treated
with 2% e-cigarette vapour condensate for 24h. Mitochondrial membrane potential was measured using
50nM TMRE (Tetramethyl rhodamine ethyl ester) and cells were visualized on ImageXpress® Pico Automated Cell Imaging System (Molecular Devices, San Jose, CA, USA) with a 10x objective.
Results: We found a significant reduction of TMRE fluorescence in treated cells compared to the control. Imaging of treated cells also revealed changes in cell morphology and the presence of mitochondria in TNT-like structures.
Conclusion: Mitochondrial dysfunction has been associated with various pathological conditions including lung diseases such as asthma, COPD and lung cancer. Due to their relative novelty, the role of
electronic cigarette use in development of chronic lung diseasesisstill relatively unknown. Our findings
contribute to the growing list of studies pointing to their adverse biological effects and imply their involvement in processes contributing to chronic lung diseases.",
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 = "Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell",
pages = "139-139",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2130"
}

Ljujić, M., Trifunović, S., Ilić, B., Milovanović, J., Dinić, J.,& Divac Rankov, A.. (2023). Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell. 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., 139-139.
https://hdl.handle.net/21.15107/rcub_imagine_2130

Ljujić M, Trifunović S, Ilić B, Milovanović J, Dinić J, Divac Rankov A. Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell. 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;:139-139.
https://hdl.handle.net/21.15107/rcub_imagine_2130 .

Ljujić, Mila, Trifunović, Sara, Ilić, Bojan, Milovanović, Jelena, Dinić, Jelena, Divac Rankov, Aleksandra, "Electronic cigarette vapour condensate affects mitochondrial potential in BEAS2B cell" 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):139-139,
https://hdl.handle.net/21.15107/rcub_imagine_2130 .

TY  - CONF
AU  - Ljujić, Mila
AU  - Milovanović, Jelena
AU  - Ilić, Bojan
AU  - Trifunović, Sara
AU  - Divac Rankov, Aleksandra
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2131
AB  - Introduction: E-cigarettes are becoming increasingly popular, but their potentially harmful effects are
not well studied. Although they are used to aid smoking cessation, there is evidence that the chemicals
they contain can affect lung cells, and the effects may also be important for lung cancer cells. Our objective wasto investigate the effects of e-cigarette vapor condensate on mitochondrial function of A549
cells.
Methods: We used the Agilent Seahorse Mito Stress Test, according to the manufacturer’s protocol to
evaluate the mitochondrial function of A549 cells under the treatment with different concentrations of
e-cigarette vapor condensates. Vapor condensates were prepared from e-cigarette liquid base (PG/VG),
base with nicotine (PG/VG+N), with flavoring (PG/VG+F), or with nicotine and flavoring (PG /VG+F+N).
The cells were exposed to 2% or 3% PG /VG, PG /VG+F, PG/VG+N, and PG/VG+F+N for 24 hours before
testing.
Results: All treatments with 2% vapor condensates affected mitochondrial function of A549 cells. Basal
and maximal respiration were decreased, indicating mitochondrial dysfunction. Higher concentrations
of vapor condensate (3%) significantly increased proton leak and decreased mitochondrial coupling efficiency, indicating mitochondrial damage. However, the increased spare respiratory capacity, in 3%
vapor condensate treated cells, may indicate activation of a compensatory response in mitochondria.
Conclusion: Our resultssuggest that e-cigarette vapor condensate may have deleterious effects on mitochondria. Further analysis of mitochondrial function and morphology would further elucidate the effects of e-cigarette vapor condensate.
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  - E-cigarette vapor condensate affects mitochondrial function in A549 cells
EP  - 140
SP  - 140
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2131
ER  - 

@conference{
author = "Ljujić, Mila and Milovanović, Jelena and Ilić, Bojan and Trifunović, Sara and Divac Rankov, Aleksandra",
year = "2023",
abstract = "Introduction: E-cigarettes are becoming increasingly popular, but their potentially harmful effects are
not well studied. Although they are used to aid smoking cessation, there is evidence that the chemicals
they contain can affect lung cells, and the effects may also be important for lung cancer cells. Our objective wasto investigate the effects of e-cigarette vapor condensate on mitochondrial function of A549
cells.
Methods: We used the Agilent Seahorse Mito Stress Test, according to the manufacturer’s protocol to
evaluate the mitochondrial function of A549 cells under the treatment with different concentrations of
e-cigarette vapor condensates. Vapor condensates were prepared from e-cigarette liquid base (PG/VG),
base with nicotine (PG/VG+N), with flavoring (PG/VG+F), or with nicotine and flavoring (PG /VG+F+N).
The cells were exposed to 2% or 3% PG /VG, PG /VG+F, PG/VG+N, and PG/VG+F+N for 24 hours before
testing.
Results: All treatments with 2% vapor condensates affected mitochondrial function of A549 cells. Basal
and maximal respiration were decreased, indicating mitochondrial dysfunction. Higher concentrations
of vapor condensate (3%) significantly increased proton leak and decreased mitochondrial coupling efficiency, indicating mitochondrial damage. However, the increased spare respiratory capacity, in 3%
vapor condensate treated cells, may indicate activation of a compensatory response in mitochondria.
Conclusion: Our resultssuggest that e-cigarette vapor condensate may have deleterious effects on mitochondria. Further analysis of mitochondrial function and morphology would further elucidate the effects of e-cigarette vapor condensate.",
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 = "E-cigarette vapor condensate affects mitochondrial function in A549 cells",
pages = "140-140",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2131"
}

Ljujić, M., Milovanović, J., Ilić, B., Trifunović, S.,& Divac Rankov, A.. (2023). E-cigarette vapor condensate affects mitochondrial function in A549 cells. 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., 140-140.
https://hdl.handle.net/21.15107/rcub_imagine_2131

Ljujić M, Milovanović J, Ilić B, Trifunović S, Divac Rankov A. E-cigarette vapor condensate affects mitochondrial function in A549 cells. 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;:140-140.
https://hdl.handle.net/21.15107/rcub_imagine_2131 .

Ljujić, Mila, Milovanović, Jelena, Ilić, Bojan, Trifunović, Sara, Divac Rankov, Aleksandra, "E-cigarette vapor condensate affects mitochondrial function in A549 cells" 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):140-140,
https://hdl.handle.net/21.15107/rcub_imagine_2131 .

TY  - CONF
AU  - Ilić, Bojan
AU  - Ljujić, Mila
AU  - Trifunović, Sara
AU  - Divac Rankov, Aleksandra
PY  - 2023
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/2120
AB  - Introduction: E-cigarettes are advertised as safer alternative to tradicional cigarettes. However, they
contain chemicals that can exhibit toxic effects on the organism. Notably, effects of e-cigarettes on in
utero development are not well studied. We wanted to compare potential toxic effects of e-cigarette liquid and vapor condensate on development of zebrafish embryos.
Methods: Six hour old zebrafish embryos were exposed to different concentrations of e-cigarette liquid
or vapour condensate – 0.1% and 1%. Untreated embryos were used as control. Each treatment and control were set up in triplicate, with at least 20 embryos per treatment. The effects on survival, hatching and
developmental malformations were monitored using light microscopy, at 3 timepoints - 24, 48 and 72
hours post fertilization (hpf).
Results: No noticeable differences between control and treated groups were observed 24 hpf. Hatched
larvae (35%) treated with 0.1% condensate had scoliosis and malformations- yolk sac and pericardial
edema at 48 hpf. In groups treated with 1% of condensate or liquid, hatching was delayed and did not
start 48 hpf. At 72 hpf timepoint, in wells with 1% condensate, less than 30% of larvae hatched in total,
which was comparable to wells with e-cigarette liquid (25%). Malformations that were observed in all
treatements are hemagglutionation, pericardial or yolk sac edema, and scoliosis. In groups with 0.1%
condensate these maformations were observed in lower number of embryos, but the percentage of
hatched larvae was higher (approximately 80%) at 72 hpf.
Conclusions: Chronic exposure to e-cigarette vapor condensate and liquid leads to severe disorders of
zebrafish embryonic 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  - E-cigarette liquid and condensate leads to impaired embryonic development of zebrafish
EP  - 73
SP  - 73
UR  - https://hdl.handle.net/21.15107/rcub_imagine_2120
ER  - 

@conference{
author = "Ilić, Bojan and Ljujić, Mila and Trifunović, Sara and Divac Rankov, Aleksandra",
year = "2023",
abstract = "Introduction: E-cigarettes are advertised as safer alternative to tradicional cigarettes. However, they
contain chemicals that can exhibit toxic effects on the organism. Notably, effects of e-cigarettes on in
utero development are not well studied. We wanted to compare potential toxic effects of e-cigarette liquid and vapor condensate on development of zebrafish embryos.
Methods: Six hour old zebrafish embryos were exposed to different concentrations of e-cigarette liquid
or vapour condensate – 0.1% and 1%. Untreated embryos were used as control. Each treatment and control were set up in triplicate, with at least 20 embryos per treatment. The effects on survival, hatching and
developmental malformations were monitored using light microscopy, at 3 timepoints - 24, 48 and 72
hours post fertilization (hpf).
Results: No noticeable differences between control and treated groups were observed 24 hpf. Hatched
larvae (35%) treated with 0.1% condensate had scoliosis and malformations- yolk sac and pericardial
edema at 48 hpf. In groups treated with 1% of condensate or liquid, hatching was delayed and did not
start 48 hpf. At 72 hpf timepoint, in wells with 1% condensate, less than 30% of larvae hatched in total,
which was comparable to wells with e-cigarette liquid (25%). Malformations that were observed in all
treatements are hemagglutionation, pericardial or yolk sac edema, and scoliosis. In groups with 0.1%
condensate these maformations were observed in lower number of embryos, but the percentage of
hatched larvae was higher (approximately 80%) at 72 hpf.
Conclusions: Chronic exposure to e-cigarette vapor condensate and liquid leads to severe disorders of
zebrafish embryonic 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 = "E-cigarette liquid and condensate leads to impaired embryonic development of zebrafish",
pages = "73-73",
url = "https://hdl.handle.net/21.15107/rcub_imagine_2120"
}

Ilić, B., Ljujić, M., Trifunović, S.,& Divac Rankov, A.. (2023). E-cigarette liquid and condensate leads to impaired embryonic development of zebrafish. 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., 73-73.
https://hdl.handle.net/21.15107/rcub_imagine_2120

Ilić B, Ljujić M, Trifunović S, Divac Rankov A. E-cigarette liquid and condensate leads to impaired embryonic development of zebrafish. 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;:73-73.
https://hdl.handle.net/21.15107/rcub_imagine_2120 .

Ilić, Bojan, Ljujić, Mila, Trifunović, Sara, Divac Rankov, Aleksandra, "E-cigarette liquid and condensate leads to impaired embryonic development of zebrafish" 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):73-73,
https://hdl.handle.net/21.15107/rcub_imagine_2120 .

TY  - CONF
AU  - Ljujić, Mila
AU  - Ilić, Bojan
AU  - Pavlović, Danica
AU  - Rabasović, Mihajlo
AU  - Divac Rankov, Aleksandra
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1734
AB  - Komplikacije sa zarastanjem rana i formiranje ožiljnog tkiva predstavljaju
globalni zdravstveni i ekonomski problem. Postoji evidentna potreba za
razvijanjem novih, efikasnih terapija koje bi poboljšale proces zarastanja rana i
transformisale ga u regenerativni proces. Alfa-1 antitripsin (AAT) je
multifunkcionalni protein koji učestvuje u različitim procesima značajnim za
zarastanje rana i regeneraciju – proliferaciji, migraciji, apoptozi i
inflamaciji. Zebrica (Danio rerio) predstavlja značajan model za istraživanja
procesa zarastanja rana, jer ima sposobnost potpune regeneracije amputiranog
repnog peraja. Cilj ovog rada je bio da se ispita uticaj proteina AAT na
regeneraciju repnog peraja embriona zebrice. Embrionima zebrice starim 48 sati
amputirano je repno peraje i zatim merena dužina repa posle 48 h pod tretmanom
(2 mg/ml AAT) i bez njega. Analizirana je ekspresija fibronektina 1a i 1b, dok je
formiranje kolagena analizirano korišćenjem drugog harmonika, nelinearnom
mikroskopijom. Pokazano je da je dužina regenerisanog dela repa veća kada su
embrioni tretirani AAT-om. Ekspresija fibronektina 1a je povećana pod
tretmanom. Primećen je trend povećanja dužine i debljine kolagenskih vlakana
pri tretmanu, što dalje podržava rezultate o podsticanju regeneracije pod
delovanjem AAT. Dobijeni rezultati ukazuju na značajan uticaj alfa-1
antitripsina na brzinu regeneracije repa embriona zebrice. S obzorom da je AAT
odobren kao lek postoji i potencijal da se njegova primena proširi i na lečenje
rana kod ljudi.
AB  - Компликације са зарастањем рана и формирање ожиљног ткива представљају
глобални здравствени и економски проблем. Постоји евидентна потреба за
развијањем нових, ефикасних терапија које би побољшале процес зарастања рана и
трансформисале га у регенеративни процес. Алфа-1 антитрипсин (ААТ) је
мултифункционални протеин који учествује у различитим процесима значајним за
зарастањe рана и регенерацију – пролиферацији, миграцији, апоптози и
инфламацији. Зебрица (Danio rerio) представља значајан модел за истраживања
процеса зарастања рана, јер има способност потпуне регенерације ампутираног
репног пераја. Циљ овог рада је био да се испита утицај протеина ААТ на
регенерацију репног пераја ембриона зебрице. Ембрионима зебрице старим 48 сати
ампутирано је репно пераје и затим мерена дужина репа после 48 h под третманом
(2 мг/мл ААТ) и без њега. Aнализирана је експресија фибронектина 1а и 1b, док је
формирање колагена анализирано коришћењем другог хармоника, нелинеарном
микроскопијом. Показано је да је дужина регенерисаног дела репа већа када су
ембриони третирани ААТ-ом. Експресија фибронектина 1а је повећана под
третманом. Примећен је тренд повећања дужине и дебљине колагенских влакана
при третману, што даље подржава резултате о подстицању регенерације под
деловањем ААТ. Добијени резултати указују на значајан утицај алфа-1
антитрипсина на брзину регенерације репа ембриона зебрице. С обзором да је ААТ
одобрен као лек постоји и потенцијал да се његова примена прошири и на лечење
рана код људи.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Alfa-1 antitripsin podstiče regenerciju repnog peraja embriona zebrice (Danio rerio)
T1  - Алфа-1 антитрипсин подстиче регенерцију репног пераја ембриона зебрице (Danio rerio)
SP  - 314
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1734
ER  - 

@conference{
author = "Ljujić, Mila and Ilić, Bojan and Pavlović, Danica and Rabasović, Mihajlo and Divac Rankov, Aleksandra",
year = "2022",
abstract = "Komplikacije sa zarastanjem rana i formiranje ožiljnog tkiva predstavljaju
globalni zdravstveni i ekonomski problem. Postoji evidentna potreba za
razvijanjem novih, efikasnih terapija koje bi poboljšale proces zarastanja rana i
transformisale ga u regenerativni proces. Alfa-1 antitripsin (AAT) je
multifunkcionalni protein koji učestvuje u različitim procesima značajnim za
zarastanje rana i regeneraciju – proliferaciji, migraciji, apoptozi i
inflamaciji. Zebrica (Danio rerio) predstavlja značajan model za istraživanja
procesa zarastanja rana, jer ima sposobnost potpune regeneracije amputiranog
repnog peraja. Cilj ovog rada je bio da se ispita uticaj proteina AAT na
regeneraciju repnog peraja embriona zebrice. Embrionima zebrice starim 48 sati
amputirano je repno peraje i zatim merena dužina repa posle 48 h pod tretmanom
(2 mg/ml AAT) i bez njega. Analizirana je ekspresija fibronektina 1a i 1b, dok je
formiranje kolagena analizirano korišćenjem drugog harmonika, nelinearnom
mikroskopijom. Pokazano je da je dužina regenerisanog dela repa veća kada su
embrioni tretirani AAT-om. Ekspresija fibronektina 1a je povećana pod
tretmanom. Primećen je trend povećanja dužine i debljine kolagenskih vlakana
pri tretmanu, što dalje podržava rezultate o podsticanju regeneracije pod
delovanjem AAT. Dobijeni rezultati ukazuju na značajan uticaj alfa-1
antitripsina na brzinu regeneracije repa embriona zebrice. S obzorom da je AAT
odobren kao lek postoji i potencijal da se njegova primena proširi i na lečenje
rana kod ljudi., Компликације са зарастањем рана и формирање ожиљног ткива представљају
глобални здравствени и економски проблем. Постоји евидентна потреба за
развијањем нових, ефикасних терапија које би побољшале процес зарастања рана и
трансформисале га у регенеративни процес. Алфа-1 антитрипсин (ААТ) је
мултифункционални протеин који учествује у различитим процесима значајним за
зарастањe рана и регенерацију – пролиферацији, миграцији, апоптози и
инфламацији. Зебрица (Danio rerio) представља значајан модел за истраживања
процеса зарастања рана, јер има способност потпуне регенерације ампутираног
репног пераја. Циљ овог рада је био да се испита утицај протеина ААТ на
регенерацију репног пераја ембриона зебрице. Ембрионима зебрице старим 48 сати
ампутирано је репно пераје и затим мерена дужина репа после 48 h под третманом
(2 мг/мл ААТ) и без њега. Aнализирана је експресија фибронектина 1а и 1b, док је
формирање колагена анализирано коришћењем другог хармоника, нелинеарном
микроскопијом. Показано је да је дужина регенерисаног дела репа већа када су
ембриони третирани ААТ-ом. Експресија фибронектина 1а је повећана под
третманом. Примећен је тренд повећања дужине и дебљине колагенских влакана
при третману, што даље подржава резултате о подстицању регенерације под
деловањем ААТ. Добијени резултати указују на значајан утицај алфа-1
антитрипсина на брзину регенерације репа ембриона зебрице. С обзором да је ААТ
одобрен као лек постоји и потенцијал да се његова примена прошири и на лечење
рана код људи.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Alfa-1 antitripsin podstiče regenerciju repnog peraja embriona zebrice (Danio rerio), Алфа-1 антитрипсин подстиче регенерцију репног пераја ембриона зебрице (Danio rerio)",
pages = "314",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1734"
}

Ljujić, M., Ilić, B., Pavlović, D., Rabasović, M.,& Divac Rankov, A.. (2022). Alfa-1 antitripsin podstiče regenerciju repnog peraja embriona zebrice (Danio rerio). in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 314.
https://hdl.handle.net/21.15107/rcub_imagine_1734

Ljujić M, Ilić B, Pavlović D, Rabasović M, Divac Rankov A. Alfa-1 antitripsin podstiče regenerciju repnog peraja embriona zebrice (Danio rerio). in Treći kongres biologa Srbije. 2022;:314.
https://hdl.handle.net/21.15107/rcub_imagine_1734 .

Ljujić, Mila, Ilić, Bojan, Pavlović, Danica, Rabasović, Mihajlo, Divac Rankov, Aleksandra, "Alfa-1 antitripsin podstiče regenerciju repnog peraja embriona zebrice (Danio rerio)" in Treći kongres biologa Srbije (2022):314,
https://hdl.handle.net/21.15107/rcub_imagine_1734 .

TY  - CONF
AU  - Jovanović Stojanov, Sofija
AU  - Kostić, Ana
AU  - Ljujić, Mila
AU  - Lupšić, Ema
AU  - Dragoj, Miodrag
AU  - Jovanović, Mirna
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1736
AB  - Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora.
AB  - Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.
PB  - Beograd : Srpsko biološko društvo
C3  - Treći kongres biologa Srbije
T1  - Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306
T1  - Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306
SP  - 330
UR  - https://hdl.handle.net/21.15107/rcub_imagine_1736
ER  - 

@conference{
author = "Jovanović Stojanov, Sofija and Kostić, Ana and Ljujić, Mila and Lupšić, Ema and Dragoj, Miodrag and Jovanović, Mirna and Pešić, Milica and Dinić, Jelena",
year = "2022",
abstract = "Glioblastom je jedan od najagresivnijih tumora mozga koji karakteriše
infiltrirajuća priroda, intenzivna proliferacija i rezistencija na terapiju.
Ćelije glioblastoma imaju visoku ekspresiju Src tirozin-kinaze koja reguliše
proliferaciju, preživljavanje i invazivnost tumorskih ćelija čineći je
potencijalnom metom za terapiju. Inhibitori tirozin-kinaza mogu indukovati
autofagiju koja deluje protektivno na tumorske ćelije. Sposobnost inhibitora
Src tirozin-kinaze, derivata pirazolo[3,4-d]pirimidina Si306 i njegovog proleka
pro-Si306, da indukuju autofagiju ispitana je na ćelijskoj liniji humanog
glioblastoma U87 i njenoj varijanti sa višestrukom rezistencijom na lekove
U87-TxR. Tretman ovim jedinjenjima uzrokovao je pojavu autofagozoma u ćelijama
nakon 3 sata, a efekat na indukciju autofagije opstao je i nakon 48 sati što je
utvrđeno analizom markera autofagije LC3 i p62. Inhibicija autofagnog fluksa
bafilomicinom A1 značajno je uvećala postojeće anti-proliferativno dejstvo
Si306 i pro-Si306. Takođe, kombinovani tretmani Src inhibitora sa
bafilomicinom A1 doveli su do nekroze nakon 48 sati. Dobijeni rezultati
sugerišu da autofagija indukovana ovim jedinjenjima ima zaštitnu ulogu u
ćelijama glioblastoma i da se modulacija autofagije može koristiti za
senzitizaciju ćelija glioblastoma na inhibitore Src tirozin-kinaze. Pored toga,
pomenuti efekti Si306 i pro-Si306 nisu umanjeni prisustvom višestruko-
rezistentnog fenotipa, što ovim jedinjenjima daje potencijal za lečenje
rezistentnih tumora., Глиобластом је један од најагресивнијих тумора мозга који карактерише
инфилтрирајућа природа, интензивна пролиферација и резистенција на терапију.
Ћелије глиобластома имају високу експресију Срц тирозин-киназе која регулише
пролиферацију, преживљавање и инвазивност туморских ћелија чинећи је
потенцијалном метом за терапију. Инхибитори тирозин-киназа могу индуковати
аутофагију која делује протективно на туморске ћелије. Способност инхибитора
Срц тирозин-киназе, деривата пиразоло[3,4-д]пиримидина Si306 и његовог пролека
pro-Si306, да индукују аутофагију испитана је на ћелијској линији хуманог
глиобластома U87 и њеној варијанти са вишеструком резистенцијом на лекове
U87-TxR. Третман овим једињењима узроковао је појаву аутофагозома у ћелијама
након 3 сата, а ефекат на индукцију аутофагије опстао је и након 48 сати што је
утврђено анализом маркера аутофагије LC3 и p62. Инхибиција аутофагног флукса
бафиломицином А1 значајно је увећала постојеће анти-пролиферативно дејство
Si306 и pro-Si306. Такође, комбиновани третмани Срц инхибитора са
бафиломицином А1 довели су до некрозе након 48 сати. Добијени резултати
сугеришу да аутофагија индукована овим једињењима има заштитну улогу у
ћелијама глиобластома и да се модулација аутофагије може користити за
сензитизацију ћелија глиобластома на инхибиторе Срц тирозин-киназе. Поред тога,
поменути ефекти Si306 и pro-Si306 нису умањени присуством вишеструко-
резистентног фенотипа, што овим једињењима даје потенцијал за лечење
резистентних тумора.",
publisher = "Beograd : Srpsko biološko društvo",
journal = "Treći kongres biologa Srbije",
title = "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306, Инхибиција аутофагије сензитизује ћелије глиобластома на инхибиторе Срц тирозин-киназе, деривате пиразоло[3,4- д]пиримидина Si306 и pro-Si306",
pages = "330",
url = "https://hdl.handle.net/21.15107/rcub_imagine_1736"
}

Jovanović Stojanov, S., Kostić, A., Ljujić, M., Lupšić, E., Dragoj, M., Jovanović, M., Pešić, M.,& Dinić, J.. (2022). Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije
Beograd : Srpsko biološko društvo., 330.
https://hdl.handle.net/21.15107/rcub_imagine_1736

Jovanović Stojanov S, Kostić A, Ljujić M, Lupšić E, Dragoj M, Jovanović M, Pešić M, Dinić J. Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306. in Treći kongres biologa Srbije. 2022;:330.
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

Jovanović Stojanov, Sofija, Kostić, Ana, Ljujić, Mila, Lupšić, Ema, Dragoj, Miodrag, Jovanović, Mirna, Pešić, Milica, Dinić, Jelena, "Inhibicija autofagije senzitizuje ćelije glioblastoma na inhibitore Src tirozin-kinaze, derivate pirazolo[3,4- d]pirimidina Si306 i pro-Si306" in Treći kongres biologa Srbije (2022):330,
https://hdl.handle.net/21.15107/rcub_imagine_1736 .

TY  - JOUR
AU  - Jovanović Stojanov, Sofija
AU  - Kostić, Ana
AU  - Ljujić, Mila
AU  - Lupšić, Ema
AU  - Schenone, Silvia
AU  - Pešić, Milica
AU  - Dinić, Jelena
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1656
AB  - Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibition by bafilomycin A1. Combined treatments of Si306 and pro-Si306 with bafilomycin A1 were synergistic in nature, and the inhibition of autophagy sensitized glioblastoma cells to Src tyrosine kinase inhibitors. Si306 and pro-Si306 more strongly inhibited cell proliferation and triggered necrosis in combination with bafilomycin A1. Our findings suggest that modulation of Si306- and pro-Si306-induced autophagy can be used to enhance the anticancer effects of these Src tyrosine kinase inhibitors and overcome the drug-resistant phenotype in glioblastoma cells.
T2  - Life
T2  - Life
T1  - Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors
IS  - 10
SP  - 1503
VL  - 12
DO  - 10.3390/life12101503
ER  - 

@article{
author = "Jovanović Stojanov, Sofija and Kostić, Ana and Ljujić, Mila and Lupšić, Ema and Schenone, Silvia and Pešić, Milica and Dinić, Jelena",
year = "2022",
abstract = "Drug resistance presents a major obstacle to the successful treatment of glioblastoma. Autophagy plays a key role in drug resistance, particularly in relation to targeted therapy, which has prompted the use of autophagy inhibitors to increase the effectiveness of targeted therapeutics. The ability of two Src tyrosine kinase inhibitors, Si306 and its prodrug pro-Si306, to induce autophagy was evaluated in the human glioblastoma cell line U87 and its multidrug-resistant counterpart U87-TxR. Autophagy markers were assessed by flow cytometry, microscopy, and Western blot, and induction of autophagy by these compounds was demonstrated after 3 h as well as 48 h. The effects of Si306 and pro-Si306 on cell proliferation and cell death were examined in the presence or absence of autophagy inhibition by bafilomycin A1. Combined treatments of Si306 and pro-Si306 with bafilomycin A1 were synergistic in nature, and the inhibition of autophagy sensitized glioblastoma cells to Src tyrosine kinase inhibitors. Si306 and pro-Si306 more strongly inhibited cell proliferation and triggered necrosis in combination with bafilomycin A1. Our findings suggest that modulation of Si306- and pro-Si306-induced autophagy can be used to enhance the anticancer effects of these Src tyrosine kinase inhibitors and overcome the drug-resistant phenotype in glioblastoma cells.",
journal = "Life, Life",
title = "Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors",
number = "10",
pages = "1503",
volume = "12",
doi = "10.3390/life12101503"
}

Jovanović Stojanov, S., Kostić, A., Ljujić, M., Lupšić, E., Schenone, S., Pešić, M.,& Dinić, J.. (2022). Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors. in Life, 12(10), 1503.
https://doi.org/10.3390/life12101503

Jovanović Stojanov S, Kostić A, Ljujić M, Lupšić E, Schenone S, Pešić M, Dinić J. Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors. in Life. 2022;12(10):1503.
doi:10.3390/life12101503 .

Jovanović Stojanov, Sofija, Kostić, Ana, Ljujić, Mila, Lupšić, Ema, Schenone, Silvia, Pešić, Milica, Dinić, Jelena, "Autophagy Inhibition Enhances Anti-Glioblastoma Effects of Pyrazolo[3,4-d]pyrimidine Tyrosine Kinase Inhibitors" in Life, 12, no. 10 (2022):1503,
https://doi.org/10.3390/life12101503 . .

TY  - JOUR
AU  - Trifunović, Sara
AU  - Smiljanić, Katarina
AU  - Sickmann, Albert
AU  - Solari, Fiorella A.
AU  - Kolarević, Stoimir
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1583
AB  - Background Although still considered a safer alternative to classical cigarettes, growing body of work points to harmful effects of electronic cigarettes (e-cigarettes) affecting a range of cellular processes. The biological effect of e-cigarettes needs to be investigated in more detail considering their widespread use. Methods In this study, we treated V79 lung fibroblasts with sub-cytotoxic concentration of e-cigarette liquids, with and without nicotine. Mutagenicity was evaluated by HPRT assay, genotoxicity by comet assay and the effect on cellular communication by metabolic cooperation assay. Additionally, comprehensive proteome analysis was performed via high resolution, parallel accumulation serial fragmentation-PASEF mass spectrometry. Results E-cigarette liquid concentration used in this study showed no mutagenic or genotoxic effect, however it negatively impacted metabolic cooperation between V79 cells. Both e-cigarette liquids induced significant depletion in total number of proteins and impairment of mitochondrial function in treated cells. The focal adhesion proteins were upregulated, which is in accordance with the results of metabolic cooperation assay. Increased presence of posttranslational modifications (PTMs), including carbonylation and direct oxidative modifications, was observed. Data are available via ProteomeXchange with identifier PXD032071. Conclusions Our study revealed impairment of metabolic cooperation as well as significant proteome and PTMs alterations in V79 cells treated with e-cigarette liquid warranting future studies on e-cigarettes health impact.
PB  - BMC, London
T2  - Respiratory Research
T1  - Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells
IS  - 1
VL  - 23
DO  - 10.1186/s12931-022-02102-w
ER  - 

@article{
author = "Trifunović, Sara and Smiljanić, Katarina and Sickmann, Albert and Solari, Fiorella A. and Kolarević, Stoimir and Divac Rankov, Aleksandra and Ljujić, Mila",
year = "2022",
abstract = "Background Although still considered a safer alternative to classical cigarettes, growing body of work points to harmful effects of electronic cigarettes (e-cigarettes) affecting a range of cellular processes. The biological effect of e-cigarettes needs to be investigated in more detail considering their widespread use. Methods In this study, we treated V79 lung fibroblasts with sub-cytotoxic concentration of e-cigarette liquids, with and without nicotine. Mutagenicity was evaluated by HPRT assay, genotoxicity by comet assay and the effect on cellular communication by metabolic cooperation assay. Additionally, comprehensive proteome analysis was performed via high resolution, parallel accumulation serial fragmentation-PASEF mass spectrometry. Results E-cigarette liquid concentration used in this study showed no mutagenic or genotoxic effect, however it negatively impacted metabolic cooperation between V79 cells. Both e-cigarette liquids induced significant depletion in total number of proteins and impairment of mitochondrial function in treated cells. The focal adhesion proteins were upregulated, which is in accordance with the results of metabolic cooperation assay. Increased presence of posttranslational modifications (PTMs), including carbonylation and direct oxidative modifications, was observed. Data are available via ProteomeXchange with identifier PXD032071. Conclusions Our study revealed impairment of metabolic cooperation as well as significant proteome and PTMs alterations in V79 cells treated with e-cigarette liquid warranting future studies on e-cigarettes health impact.",
publisher = "BMC, London",
journal = "Respiratory Research",
title = "Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells",
number = "1",
volume = "23",
doi = "10.1186/s12931-022-02102-w"
}

Trifunović, S., Smiljanić, K., Sickmann, A., Solari, F. A., Kolarević, S., Divac Rankov, A.,& Ljujić, M.. (2022). Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells. in Respiratory Research
BMC, London., 23(1).
https://doi.org/10.1186/s12931-022-02102-w

Trifunović S, Smiljanić K, Sickmann A, Solari FA, Kolarević S, Divac Rankov A, Ljujić M. Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells. in Respiratory Research. 2022;23(1).
doi:10.1186/s12931-022-02102-w .

Trifunović, Sara, Smiljanić, Katarina, Sickmann, Albert, Solari, Fiorella A., Kolarević, Stoimir, Divac Rankov, Aleksandra, Ljujić, Mila, "Electronic cigarette liquids impair metabolic cooperation and alter proteomic profiles in V79 cells" in Respiratory Research, 23, no. 1 (2022),
https://doi.org/10.1186/s12931-022-02102-w . .

TY  - JOUR
AU  - Jovanović, Mirna
AU  - Stanković, Tijana
AU  - Stojković Burić, Sonja
AU  - Banković, Jasna
AU  - Dinić, Jelena
AU  - Ljujić, Mila
AU  - Pesić, Milica
AU  - Dragoj, Miodrag
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1526
AB  - Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.
PB  - MDPI, Basel
T2  - Life-Basel
T1  - Decreased TSPAN14 Expression Contributes to NSCLC Progression
IS  - 9
VL  - 12
DO  - 10.3390/life12091291
ER  - 

@article{
author = "Jovanović, Mirna and Stanković, Tijana and Stojković Burić, Sonja and Banković, Jasna and Dinić, Jelena and Ljujić, Mila and Pesić, Milica and Dragoj, Miodrag",
year = "2022",
abstract = "Tspan14 is a transmembrane protein of the tetraspanin (Tspan) protein family. Different members of the Tspan family can promote or suppress tumor progression. The exact role of Tspan14 in tumor cells is unknown. Earlier, mutational inactivation of the TSPAN14 gene has been proposed to coincide with a low survival rate in NSCLC patients. This study aimed to investigate the correlation of TSPAN14 lack of function with clinicopathological features of NSCLC patients, and to elucidate the role TSPAN14 might have in NSCLC progression. TSPAN14 expression was lower in tumor cells than non-tumor cells in NSCLC patients' samples. The decreased gene expression was correlated with a low survival rate of patients and was more frequent in patients with aggressive, invasive tumor types. Additionally, the role of decreased TSPAN14 expression in the metastatic potential of cancer cells was confirmed in NSCLC cell lines. The highly invasive NSCLC cell line (NCI-H661) had the lowest TSPAN14 gene and protein expression, whereas the NSCLC cell line with the highest TSPAN14 expression (NCI-H460) had no significant metastatic potential. Finally, silencing of TSPAN14 in these non-metastatic cancer cells caused an increased expression of matrix-degrading enzymes MMP-2 and MMP-9, followed by an elevated capacity of cancer cells to degrade gelatin. The results of this study propose TSPAN14 expression as an indicator of NSCLC metastatic potential and progression.",
publisher = "MDPI, Basel",
journal = "Life-Basel",
title = "Decreased TSPAN14 Expression Contributes to NSCLC Progression",
number = "9",
volume = "12",
doi = "10.3390/life12091291"
}

Jovanović, M., Stanković, T., Stojković Burić, S., Banković, J., Dinić, J., Ljujić, M., Pesić, M.,& Dragoj, M.. (2022). Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel
MDPI, Basel., 12(9).
https://doi.org/10.3390/life12091291

Jovanović M, Stanković T, Stojković Burić S, Banković J, Dinić J, Ljujić M, Pesić M, Dragoj M. Decreased TSPAN14 Expression Contributes to NSCLC Progression. in Life-Basel. 2022;12(9).
doi:10.3390/life12091291 .

Jovanović, Mirna, Stanković, Tijana, Stojković Burić, Sonja, Banković, Jasna, Dinić, Jelena, Ljujić, Mila, Pesić, Milica, Dragoj, Miodrag, "Decreased TSPAN14 Expression Contributes to NSCLC Progression" in Life-Basel, 12, no. 9 (2022),
https://doi.org/10.3390/life12091291 . .

TY  - CONF
AU  - Beletić, Anđelo
AU  - Dudvarski-Ilić, A.
AU  - Nagorni-Obradović, L.
AU  - Milenković, B.
AU  - Ljujić, Mila
AU  - Radojković, Dragica
AU  - Đorđević, Valentina
AU  - Stanković, S.
PY  - 2022
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1597
PB  - Elsevier, Amsterdam
C3  - Clinica Chimica Acta
T1  - Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among adults - a pilot study in the Republic of Serbia
EP  - S345
SP  - S344
VL  - 530
DO  - 10.1016/j.cca.2022.04.893
ER  - 

@conference{
author = "Beletić, Anđelo and Dudvarski-Ilić, A. and Nagorni-Obradović, L. and Milenković, B. and Ljujić, Mila and Radojković, Dragica and Đorđević, Valentina and Stanković, S.",
year = "2022",
publisher = "Elsevier, Amsterdam",
journal = "Clinica Chimica Acta",
title = "Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among adults - a pilot study in the Republic of Serbia",
pages = "S345-S344",
volume = "530",
doi = "10.1016/j.cca.2022.04.893"
}

Beletić, A., Dudvarski-Ilić, A., Nagorni-Obradović, L., Milenković, B., Ljujić, M., Radojković, D., Đorđević, V.,& Stanković, S.. (2022). Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among adults - a pilot study in the Republic of Serbia. in Clinica Chimica Acta
Elsevier, Amsterdam., 530, S344-S345.
https://doi.org/10.1016/j.cca.2022.04.893

Beletić A, Dudvarski-Ilić A, Nagorni-Obradović L, Milenković B, Ljujić M, Radojković D, Đorđević V, Stanković S. Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among adults - a pilot study in the Republic of Serbia. in Clinica Chimica Acta. 2022;530:S344-S345.
doi:10.1016/j.cca.2022.04.893 .

Beletić, Anđelo, Dudvarski-Ilić, A., Nagorni-Obradović, L., Milenković, B., Ljujić, Mila, Radojković, Dragica, Đorđević, Valentina, Stanković, S., "Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among adults - a pilot study in the Republic of Serbia" in Clinica Chimica Acta, 530 (2022):S344-S345,
https://doi.org/10.1016/j.cca.2022.04.893 . .

TY  - CHAP
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1637
AB  - Estimated human genetic diversity is 0.1%, meaning that any two individuals differ at approximately one in every thousand base pairs. A small proportion of these genetic variants have functional consequences affecting health, including susceptibility to infections, diseases, and response to different drugs. Advancements in high-throughput sequencing technology have provided more insight into human genetic makeup and enabled better understanding of the link between genetic variations and health outcomes. However, despite considerable progress in human genetics, there are still many diseases that, given their complexity, cannot be explained simply by the genetic variants present and the involvement of factors such as epigenetics, environmental factors, and gene–environment interactions must be considered. We will discuss how human genetic diversity helps us to uncover the underlining mechanisms in monogenic, complex, and infectious diseases leading to a personalized approach to drug development and treatment.
PB  - Academic Press
T2  - Biodiversity and Biomedicine
T1  - Chapter 8 - Human genetic diversity in health and disease
EP  - 136
SP  - 123
DO  - 10.1016/B978-0-12-819541-3.00008-6
ER  - 

@inbook{
author = "Divac Rankov, Aleksandra and Ljujić, Mila",
year = "2020",
abstract = "Estimated human genetic diversity is 0.1%, meaning that any two individuals differ at approximately one in every thousand base pairs. A small proportion of these genetic variants have functional consequences affecting health, including susceptibility to infections, diseases, and response to different drugs. Advancements in high-throughput sequencing technology have provided more insight into human genetic makeup and enabled better understanding of the link between genetic variations and health outcomes. However, despite considerable progress in human genetics, there are still many diseases that, given their complexity, cannot be explained simply by the genetic variants present and the involvement of factors such as epigenetics, environmental factors, and gene–environment interactions must be considered. We will discuss how human genetic diversity helps us to uncover the underlining mechanisms in monogenic, complex, and infectious diseases leading to a personalized approach to drug development and treatment.",
publisher = "Academic Press",
journal = "Biodiversity and Biomedicine",
booktitle = "Chapter 8 - Human genetic diversity in health and disease",
pages = "136-123",
doi = "10.1016/B978-0-12-819541-3.00008-6"
}

Divac Rankov, A.,& Ljujić, M.. (2020). Chapter 8 - Human genetic diversity in health and disease. in Biodiversity and Biomedicine
Academic Press., 123-136.
https://doi.org/10.1016/B978-0-12-819541-3.00008-6

Divac Rankov A, Ljujić M. Chapter 8 - Human genetic diversity in health and disease. in Biodiversity and Biomedicine. 2020;:123-136.
doi:10.1016/B978-0-12-819541-3.00008-6 .

Divac Rankov, Aleksandra, Ljujić, Mila, "Chapter 8 - Human genetic diversity in health and disease" in Biodiversity and Biomedicine (2020):123-136,
https://doi.org/10.1016/B978-0-12-819541-3.00008-6 . .

TY  - JOUR
AU  - Talty, Aaron
AU  - Deegan, Shane
AU  - Ljujić, Mila
AU  - Mnich, Katarzyna
AU  - Naicker, Serika D.
AU  - Quandt, Dagmar
AU  - Zeng, Qingping
AU  - Patterson, John B.
AU  - Gorman, Adrienne M.
AU  - Griffin, Matthew D.
AU  - Samali, Afshin
AU  - Logue, Susan E.
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1379
PB  - Nature Publishing Group, London
T2  - Cell Death & Disease
T1  - Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta (vol 77, pg 568, 2019)
IS  - 1
VL  - 11
DO  - 10.1038/s41419-019-2189-6
ER  - 

@article{
author = "Talty, Aaron and Deegan, Shane and Ljujić, Mila and Mnich, Katarzyna and Naicker, Serika D. and Quandt, Dagmar and Zeng, Qingping and Patterson, John B. and Gorman, Adrienne M. and Griffin, Matthew D. and Samali, Afshin and Logue, Susan E.",
year = "2020",
publisher = "Nature Publishing Group, London",
journal = "Cell Death & Disease",
title = "Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta (vol 77, pg 568, 2019)",
number = "1",
volume = "11",
doi = "10.1038/s41419-019-2189-6"
}

Talty, A., Deegan, S., Ljujić, M., Mnich, K., Naicker, S. D., Quandt, D., Zeng, Q., Patterson, J. B., Gorman, A. M., Griffin, M. D., Samali, A.,& Logue, S. E.. (2020). Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta (vol 77, pg 568, 2019). in Cell Death & Disease
Nature Publishing Group, London., 11(1).
https://doi.org/10.1038/s41419-019-2189-6

Talty A, Deegan S, Ljujić M, Mnich K, Naicker SD, Quandt D, Zeng Q, Patterson JB, Gorman AM, Griffin MD, Samali A, Logue SE. Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta (vol 77, pg 568, 2019). in Cell Death & Disease. 2020;11(1).
doi:10.1038/s41419-019-2189-6 .

Talty, Aaron, Deegan, Shane, Ljujić, Mila, Mnich, Katarzyna, Naicker, Serika D., Quandt, Dagmar, Zeng, Qingping, Patterson, John B., Gorman, Adrienne M., Griffin, Matthew D., Samali, Afshin, Logue, Susan E., "Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta (vol 77, pg 568, 2019)" in Cell Death & Disease, 11, no. 1 (2020),
https://doi.org/10.1038/s41419-019-2189-6 . .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Kušić-Tišma, Jelena
AU  - Ljujić, Mila
AU  - Nikolić, Aleksandra
AU  - Milosević, Katarina
AU  - Dautović, Gordana Vilotijevic
AU  - Radojković, Dragica
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1381
AB  - Background: High heterogeneity levels of cystic fibrosis transmembrane regulator (CFTR) are manifested in different populations. The aim of this study was to analyze comprehensively all mutations in the CFTR gene in Serbian patients with cystic fibrosis (CF) and to use the findings to propose a testing algorithm for the Serbian population. Materials and Methods: Cascade screening was employed to detect mutations in the CFTR gene of 90 patients suspected of having CF, using polymerase chain reaction (PCR), PCR-restriction fragment length polymorphism or PCR-mediated site directed mutagenesis, Sanger sequencing, and/or next-generation sequencing. Results: This is the first report for the Serbian CF population where single nucleotide polymorphisms, small insertions and deletions, large genome rearrangements, and copy number variants were analyzed in detail. A high degree of heterogeneity within the CFTR was documented among our cohort of 90 patients. We identified 19 CF-causing mutations and 3 with varying consequences, including a previously unreported deletion of the entire exon 11. Conclusion: Considering the spectrum and frequency of mutations found, we recommend a multistep sequencing algorithm in combination with evaluation of large rearrangements for future analyses of the CFTR gene in the Serbian population.
PB  - Mary Ann Liebert, Inc, New Rochelle
T2  - Genetic Testing and Molecular Biomarkers
T1  - Molecular Diagnostics of Cystic Fibrosis in Serbia: Our Approach to Meet the Diagnostic Challenges
EP  - 216
IS  - 4
SP  - 212
VL  - 24
DO  - 10.1089/gtmb.2019.0171
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Kušić-Tišma, Jelena and Ljujić, Mila and Nikolić, Aleksandra and Milosević, Katarina and Dautović, Gordana Vilotijevic and Radojković, Dragica",
year = "2020",
abstract = "Background: High heterogeneity levels of cystic fibrosis transmembrane regulator (CFTR) are manifested in different populations. The aim of this study was to analyze comprehensively all mutations in the CFTR gene in Serbian patients with cystic fibrosis (CF) and to use the findings to propose a testing algorithm for the Serbian population. Materials and Methods: Cascade screening was employed to detect mutations in the CFTR gene of 90 patients suspected of having CF, using polymerase chain reaction (PCR), PCR-restriction fragment length polymorphism or PCR-mediated site directed mutagenesis, Sanger sequencing, and/or next-generation sequencing. Results: This is the first report for the Serbian CF population where single nucleotide polymorphisms, small insertions and deletions, large genome rearrangements, and copy number variants were analyzed in detail. A high degree of heterogeneity within the CFTR was documented among our cohort of 90 patients. We identified 19 CF-causing mutations and 3 with varying consequences, including a previously unreported deletion of the entire exon 11. Conclusion: Considering the spectrum and frequency of mutations found, we recommend a multistep sequencing algorithm in combination with evaluation of large rearrangements for future analyses of the CFTR gene in the Serbian population.",
publisher = "Mary Ann Liebert, Inc, New Rochelle",
journal = "Genetic Testing and Molecular Biomarkers",
title = "Molecular Diagnostics of Cystic Fibrosis in Serbia: Our Approach to Meet the Diagnostic Challenges",
pages = "216-212",
number = "4",
volume = "24",
doi = "10.1089/gtmb.2019.0171"
}

Divac Rankov, A., Kušić-Tišma, J., Ljujić, M., Nikolić, A., Milosević, K., Dautović, G. V.,& Radojković, D.. (2020). Molecular Diagnostics of Cystic Fibrosis in Serbia: Our Approach to Meet the Diagnostic Challenges. in Genetic Testing and Molecular Biomarkers
Mary Ann Liebert, Inc, New Rochelle., 24(4), 212-216.
https://doi.org/10.1089/gtmb.2019.0171

Divac Rankov A, Kušić-Tišma J, Ljujić M, Nikolić A, Milosević K, Dautović GV, Radojković D. Molecular Diagnostics of Cystic Fibrosis in Serbia: Our Approach to Meet the Diagnostic Challenges. in Genetic Testing and Molecular Biomarkers. 2020;24(4):212-216.
doi:10.1089/gtmb.2019.0171 .

Divac Rankov, Aleksandra, Kušić-Tišma, Jelena, Ljujić, Mila, Nikolić, Aleksandra, Milosević, Katarina, Dautović, Gordana Vilotijevic, Radojković, Dragica, "Molecular Diagnostics of Cystic Fibrosis in Serbia: Our Approach to Meet the Diagnostic Challenges" in Genetic Testing and Molecular Biomarkers, 24, no. 4 (2020):212-216,
https://doi.org/10.1089/gtmb.2019.0171 . .

TY  - CONF
AU  - Divac Rankov, Aleksandra
AU  - Trifunović, Sara
AU  - Ljujić, Mila
PY  - 2020
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1334
PB  - European Respiratory Soc Journals Ltd, Sheffield
C3  - European Respiratory Journal
T1  - Electronic cigarette liquids induce formation of tunnelling nanotubes in BEAS2B cells
VL  - 56
DO  - 10.1183/13993003.congress-2020.1967
ER  - 

@conference{
author = "Divac Rankov, Aleksandra and Trifunović, Sara and Ljujić, Mila",
year = "2020",
publisher = "European Respiratory Soc Journals Ltd, Sheffield",
journal = "European Respiratory Journal",
title = "Electronic cigarette liquids induce formation of tunnelling nanotubes in BEAS2B cells",
volume = "56",
doi = "10.1183/13993003.congress-2020.1967"
}

Divac Rankov, A., Trifunović, S.,& Ljujić, M.. (2020). Electronic cigarette liquids induce formation of tunnelling nanotubes in BEAS2B cells. in European Respiratory Journal
European Respiratory Soc Journals Ltd, Sheffield., 56.
https://doi.org/10.1183/13993003.congress-2020.1967

Divac Rankov A, Trifunović S, Ljujić M. Electronic cigarette liquids induce formation of tunnelling nanotubes in BEAS2B cells. in European Respiratory Journal. 2020;56.
doi:10.1183/13993003.congress-2020.1967 .

Divac Rankov, Aleksandra, Trifunović, Sara, Ljujić, Mila, "Electronic cigarette liquids induce formation of tunnelling nanotubes in BEAS2B cells" in European Respiratory Journal, 56 (2020),
https://doi.org/10.1183/13993003.congress-2020.1967 . .

TY  - CONF
AU  - Ljujić, Mila
AU  - Vignjević, Nataša
AU  - Divac Rankov, Aleksandra
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1830
AB  - The use of electronic cigarettes is on the rise with a public perceiving them as a safer alternative to conventional cigarettes. However, their safety has only recently started being studied to a greater extent.

The aim of this study was to test the toxicity of commercially available electronic cigarette liquids (ECL) with and without nicotine in vitro and in vivo.

Two cell lines originating from the lung tissue were used - A549 and BEAS-2B. Using MTT assay, we have shown that there is a dose dependant decrease in cell viability in case of both tested liquids, and in both cell lines. We also detected cell-free mitochondrial DNA in culture medium of treated cells, indicating necrotic cell death. In order to investigate if cells undergone necroptosis we used pre-treatment with necrostatin-1 (Nec-1), a specific RIP-1 kinase inhibitor. The addition of Nec-1 did not affect cell survival under tested conditions suggesting that the cells do not go through the process of controlled necrosis.

In vivo toxicity of different concentrations of ECL was assessed by the analysis of survival, hatching and malformations of zebrafish embryos. The effects of ECL with nicotine were comparable to those when embryos were treated with pure nicotine at the same concentration, while the ECL without nicotine did not have toxic effects in used concentrations. The embryo mortality was increased when treated with ECL with 20µg/mL of nicotine and several embryo malformations (pericardial oedema, body curvature, shortening of the body and decreased movements) were present at 10µg/mL concentration.

Our result highlight the need for further testing the molecular effects and safety of electronic cigarettes.
PB  - The European Respiratory Society
C3  - European Respiratory Journal
T1  - Electronic cigarette liquids show toxic effects in vitro and in vivo
SP  - PA2444
VL  - 54
DO  - 10.1183/13993003.congress-2019.PA2444
ER  - 

@conference{
author = "Ljujić, Mila and Vignjević, Nataša and Divac Rankov, Aleksandra",
year = "2019",
abstract = "The use of electronic cigarettes is on the rise with a public perceiving them as a safer alternative to conventional cigarettes. However, their safety has only recently started being studied to a greater extent.

The aim of this study was to test the toxicity of commercially available electronic cigarette liquids (ECL) with and without nicotine in vitro and in vivo.

Two cell lines originating from the lung tissue were used - A549 and BEAS-2B. Using MTT assay, we have shown that there is a dose dependant decrease in cell viability in case of both tested liquids, and in both cell lines. We also detected cell-free mitochondrial DNA in culture medium of treated cells, indicating necrotic cell death. In order to investigate if cells undergone necroptosis we used pre-treatment with necrostatin-1 (Nec-1), a specific RIP-1 kinase inhibitor. The addition of Nec-1 did not affect cell survival under tested conditions suggesting that the cells do not go through the process of controlled necrosis.

In vivo toxicity of different concentrations of ECL was assessed by the analysis of survival, hatching and malformations of zebrafish embryos. The effects of ECL with nicotine were comparable to those when embryos were treated with pure nicotine at the same concentration, while the ECL without nicotine did not have toxic effects in used concentrations. The embryo mortality was increased when treated with ECL with 20µg/mL of nicotine and several embryo malformations (pericardial oedema, body curvature, shortening of the body and decreased movements) were present at 10µg/mL concentration.

Our result highlight the need for further testing the molecular effects and safety of electronic cigarettes.",
publisher = "The European Respiratory Society",
journal = "European Respiratory Journal",
title = "Electronic cigarette liquids show toxic effects in vitro and in vivo",
pages = "PA2444",
volume = "54",
doi = "10.1183/13993003.congress-2019.PA2444"
}

Ljujić, M., Vignjević, N.,& Divac Rankov, A.. (2019). Electronic cigarette liquids show toxic effects in vitro and in vivo. in European Respiratory Journal
The European Respiratory Society., 54, PA2444.
https://doi.org/10.1183/13993003.congress-2019.PA2444

Ljujić M, Vignjević N, Divac Rankov A. Electronic cigarette liquids show toxic effects in vitro and in vivo. in European Respiratory Journal. 2019;54:PA2444.
doi:10.1183/13993003.congress-2019.PA2444 .

Ljujić, Mila, Vignjević, Nataša, Divac Rankov, Aleksandra, "Electronic cigarette liquids show toxic effects in vitro and in vivo" in European Respiratory Journal, 54 (2019):PA2444,
https://doi.org/10.1183/13993003.congress-2019.PA2444 . .

TY  - CONF
AU  - Beletić, Anđelo
AU  - Leković, Z.
AU  - Zivković, Z.
AU  - Radlović, N.
AU  - Perisić, V.
AU  - Ljujić, Mila
AU  - Radojković, Dragica
AU  - Đorđević, Valentina
AU  - Stanković, S.
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1226
AB  - Background-aim
Alpha-1-antitrypsin deficiency (AATD) is an autosomal recessive
disorder characterized by the reduced alpha-1-antitrypsin (AAT)
level in blood. In pediatric patients, it is dominantly tested as a cause
of liver disease, while specific lung diseases might be potentially
regarded as additional indications. Measurement of AAT concentration is useful as a first-line test, although decreased level may be also
encountered in certain acquired conditions. Our aim was to
determine the interpretative cut-off for AAT concentration i.e. level
below which the presence of common AATD-associated alleles might
be suspected.
Methods
We included 37 subjects with clinical indications or familiar
history of AATD: 19 males and 18 females, aged between 2 months
and 19 years. Immunonephelometry was used for measurement of
AAT concentration in serum and PCR-reverse allele specific hybridization assay for detection of Z and S alleles, which are considered as
the common AATD-associated alleles. Kruskal-Wallis test and ROC
analysis were applied in statistical evaluation.
Results
Three cases of AATD (ZZ genotype) and 14 carriers (13
heterozygous for Z and one for S allele) were detected. AAT
concentration (median (min-max)) measured in AATD cases (0.35
(0.31–0.39) g/L), carriers (0.81 (0.56–1.41) g/L) and patients with
no Z and S allele (1.20 (0.91–2.24) g/L) were significantly different
(P b .001). Four carriers (three heterozygous for Z and one for S
allele) had AAT concentration in the reference range (0.9–2.0 g/L).
We identified the level 1.03 g/L as the most appropriate cut-off to
distinguish group comprising both cases of AATD and carriers from
patients in whom no common AATD-associated allele was present.
Corresponding AUC value (95% Confidence interval (CI)) was 0.929
(0.795–0.987) (P b .001). Sensitivity and specificity (95% CI) reached
94.1 (71.3–99.9)% and 90.0 (68.3–98.8)% respectively.
Conclusions
In pediatric patients AAT concentration below 1.03 g/L may be
regarded as a potential cut-off indicating the presence of common
AATD-associated alleles in homo-or heterozygous form. Nevertheless, this preliminary finding needs confirmation in a larger study.
PB  - Elsevier, Amsterdam
C3  - Clinica Chimica Acta
T1  - Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among pediatric patients - A pilot study
EP  - S455
SP  - S455
VL  - 493
DO  - 10.1016/j.cca.2019.03.964
ER  - 

@conference{
author = "Beletić, Anđelo and Leković, Z. and Zivković, Z. and Radlović, N. and Perisić, V. and Ljujić, Mila and Radojković, Dragica and Đorđević, Valentina and Stanković, S.",
year = "2019",
abstract = "Background-aim
Alpha-1-antitrypsin deficiency (AATD) is an autosomal recessive
disorder characterized by the reduced alpha-1-antitrypsin (AAT)
level in blood. In pediatric patients, it is dominantly tested as a cause
of liver disease, while specific lung diseases might be potentially
regarded as additional indications. Measurement of AAT concentration is useful as a first-line test, although decreased level may be also
encountered in certain acquired conditions. Our aim was to
determine the interpretative cut-off for AAT concentration i.e. level
below which the presence of common AATD-associated alleles might
be suspected.
Methods
We included 37 subjects with clinical indications or familiar
history of AATD: 19 males and 18 females, aged between 2 months
and 19 years. Immunonephelometry was used for measurement of
AAT concentration in serum and PCR-reverse allele specific hybridization assay for detection of Z and S alleles, which are considered as
the common AATD-associated alleles. Kruskal-Wallis test and ROC
analysis were applied in statistical evaluation.
Results
Three cases of AATD (ZZ genotype) and 14 carriers (13
heterozygous for Z and one for S allele) were detected. AAT
concentration (median (min-max)) measured in AATD cases (0.35
(0.31–0.39) g/L), carriers (0.81 (0.56–1.41) g/L) and patients with
no Z and S allele (1.20 (0.91–2.24) g/L) were significantly different
(P b .001). Four carriers (three heterozygous for Z and one for S
allele) had AAT concentration in the reference range (0.9–2.0 g/L).
We identified the level 1.03 g/L as the most appropriate cut-off to
distinguish group comprising both cases of AATD and carriers from
patients in whom no common AATD-associated allele was present.
Corresponding AUC value (95% Confidence interval (CI)) was 0.929
(0.795–0.987) (P b .001). Sensitivity and specificity (95% CI) reached
94.1 (71.3–99.9)% and 90.0 (68.3–98.8)% respectively.
Conclusions
In pediatric patients AAT concentration below 1.03 g/L may be
regarded as a potential cut-off indicating the presence of common
AATD-associated alleles in homo-or heterozygous form. Nevertheless, this preliminary finding needs confirmation in a larger study.",
publisher = "Elsevier, Amsterdam",
journal = "Clinica Chimica Acta",
title = "Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among pediatric patients - A pilot study",
pages = "S455-S455",
volume = "493",
doi = "10.1016/j.cca.2019.03.964"
}

Beletić, A., Leković, Z., Zivković, Z., Radlović, N., Perisić, V., Ljujić, M., Radojković, D., Đorđević, V.,& Stanković, S.. (2019). Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among pediatric patients - A pilot study. in Clinica Chimica Acta
Elsevier, Amsterdam., 493, S455-S455.
https://doi.org/10.1016/j.cca.2019.03.964

Beletić A, Leković Z, Zivković Z, Radlović N, Perisić V, Ljujić M, Radojković D, Đorđević V, Stanković S. Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among pediatric patients - A pilot study. in Clinica Chimica Acta. 2019;493:S455-S455.
doi:10.1016/j.cca.2019.03.964 .

Beletić, Anđelo, Leković, Z., Zivković, Z., Radlović, N., Perisić, V., Ljujić, Mila, Radojković, Dragica, Đorđević, Valentina, Stanković, S., "Interpretative cut-off for alpha-1-antitrypsin concentration in detection of alpha-1-antitrypsin deficiency among pediatric patients - A pilot study" in Clinica Chimica Acta, 493 (2019):S455-S455,
https://doi.org/10.1016/j.cca.2019.03.964 . .

TY  - JOUR
AU  - Talty, Aaron
AU  - Deegan, Shane
AU  - Ljujić, Mila
AU  - Mnich, Katarzyna
AU  - Naicker, Serika D.
AU  - Quandt, Dagmar
AU  - Zeng, Qingping
AU  - Patterson, John B.
AU  - Gorman, Adrienne M.
AU  - Griffin, Matthew D.
AU  - Samali, Afshin
AU  - Logue, Susan E.
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1201
AB  - The inflammasome is a multiprotein complex assembled in response to Pathogen Associated Molecular Patterns (PAMPs) and Danger Associated Molecular Patterns (DAMPS). Inflammasome activation occurs through a two-step mechanism, with the first signal facilitating priming of inflammasome components while the second signal triggers complex assembly. Once assembled, the inflammasome recruits and activates pro-caspase-1, which in turn processes pro-interleukin (IL)-18 and pro-IL-1 beta into their bio-active forms. Owing to its key role in the regulation of innate immune responses, the inflammasome has emerged as a therapeutic target for the treatment of inflammatory conditions. In this study we demonstrate that IRE1 alpha, a key component of the Unfolded Protein Response, contributes to assembly of the NLRP3 inflammasome. Blockade of IRE1 alpha RNase signaling lowered NLRP3 inflammasome assembly, caspase-1 activation and pro-IL-1 beta processing. These results underscore both the importance and potential therapeutic relevance of targeting IRE1 alpha signaling in conditions of excessive inflammasome formation.
PB  - Nature Publishing Group, London
T2  - Cell Death & Disease
T1  - Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta
VL  - 10
DO  - 10.1038/s41419-019-1847-z
ER  - 

@article{
author = "Talty, Aaron and Deegan, Shane and Ljujić, Mila and Mnich, Katarzyna and Naicker, Serika D. and Quandt, Dagmar and Zeng, Qingping and Patterson, John B. and Gorman, Adrienne M. and Griffin, Matthew D. and Samali, Afshin and Logue, Susan E.",
year = "2019",
abstract = "The inflammasome is a multiprotein complex assembled in response to Pathogen Associated Molecular Patterns (PAMPs) and Danger Associated Molecular Patterns (DAMPS). Inflammasome activation occurs through a two-step mechanism, with the first signal facilitating priming of inflammasome components while the second signal triggers complex assembly. Once assembled, the inflammasome recruits and activates pro-caspase-1, which in turn processes pro-interleukin (IL)-18 and pro-IL-1 beta into their bio-active forms. Owing to its key role in the regulation of innate immune responses, the inflammasome has emerged as a therapeutic target for the treatment of inflammatory conditions. In this study we demonstrate that IRE1 alpha, a key component of the Unfolded Protein Response, contributes to assembly of the NLRP3 inflammasome. Blockade of IRE1 alpha RNase signaling lowered NLRP3 inflammasome assembly, caspase-1 activation and pro-IL-1 beta processing. These results underscore both the importance and potential therapeutic relevance of targeting IRE1 alpha signaling in conditions of excessive inflammasome formation.",
publisher = "Nature Publishing Group, London",
journal = "Cell Death & Disease",
title = "Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta",
volume = "10",
doi = "10.1038/s41419-019-1847-z"
}

Talty, A., Deegan, S., Ljujić, M., Mnich, K., Naicker, S. D., Quandt, D., Zeng, Q., Patterson, J. B., Gorman, A. M., Griffin, M. D., Samali, A.,& Logue, S. E.. (2019). Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta. in Cell Death & Disease
Nature Publishing Group, London., 10.
https://doi.org/10.1038/s41419-019-1847-z

Talty A, Deegan S, Ljujić M, Mnich K, Naicker SD, Quandt D, Zeng Q, Patterson JB, Gorman AM, Griffin MD, Samali A, Logue SE. Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta. in Cell Death & Disease. 2019;10.
doi:10.1038/s41419-019-1847-z .

Talty, Aaron, Deegan, Shane, Ljujić, Mila, Mnich, Katarzyna, Naicker, Serika D., Quandt, Dagmar, Zeng, Qingping, Patterson, John B., Gorman, Adrienne M., Griffin, Matthew D., Samali, Afshin, Logue, Susan E., "Inhibition of IRE1 alpha RNase activity reduces NLRP3 inflammasome assembly and processing of pro-IL1 beta" in Cell Death & Disease, 10 (2019),
https://doi.org/10.1038/s41419-019-1847-z . .

TY  - CONF
AU  - Ljujić, Mila
AU  - Varga, Mate
AU  - Bartel, Sabine
AU  - Krauss-Etschmann, Susanne
AU  - Divac Rankov, Aleksandra
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1137
PB  - European Respiratory Soc Journals Ltd, Sheffield
C3  - European Respiratory Journal
T1  - Zebrafish as a model for study of developmental origins of chronic lung diseases
VL  - 52
DO  - 10.1183/13993003.congress-2018.PA1389
ER  - 

@conference{
author = "Ljujić, Mila and Varga, Mate and Bartel, Sabine and Krauss-Etschmann, Susanne and Divac Rankov, Aleksandra",
year = "2018",
publisher = "European Respiratory Soc Journals Ltd, Sheffield",
journal = "European Respiratory Journal",
title = "Zebrafish as a model for study of developmental origins of chronic lung diseases",
volume = "52",
doi = "10.1183/13993003.congress-2018.PA1389"
}

Ljujić, M., Varga, M., Bartel, S., Krauss-Etschmann, S.,& Divac Rankov, A.. (2018). Zebrafish as a model for study of developmental origins of chronic lung diseases. in European Respiratory Journal
European Respiratory Soc Journals Ltd, Sheffield., 52.
https://doi.org/10.1183/13993003.congress-2018.PA1389

Ljujić M, Varga M, Bartel S, Krauss-Etschmann S, Divac Rankov A. Zebrafish as a model for study of developmental origins of chronic lung diseases. in European Respiratory Journal. 2018;52.
doi:10.1183/13993003.congress-2018.PA1389 .

Ljujić, Mila, Varga, Mate, Bartel, Sabine, Krauss-Etschmann, Susanne, Divac Rankov, Aleksandra, "Zebrafish as a model for study of developmental origins of chronic lung diseases" in European Respiratory Journal, 52 (2018),
https://doi.org/10.1183/13993003.congress-2018.PA1389 . .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Petrić, Marija
AU  - Radojković, Dragica
AU  - Pesić, Milica
AU  - Dinić, Jelena
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1758
AB  - Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.
PB  - Springer, New York
T2  - Histochemistry and Cell Biology
T1  - Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells
EP  - 544
IS  - 5
SP  - 529
VL  - 148
DO  - 10.1007/s00418-017-1590-4
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Ljujić, Mila and Petrić, Marija and Radojković, Dragica and Pesić, Milica and Dinić, Jelena",
year = "2017",
abstract = "Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.",
publisher = "Springer, New York",
journal = "Histochemistry and Cell Biology",
title = "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells",
pages = "544-529",
number = "5",
volume = "148",
doi = "10.1007/s00418-017-1590-4"
}

Divac Rankov, A., Ljujić, M., Petrić, M., Radojković, D., Pesić, M.,& Dinić, J.. (2017). Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology
Springer, New York., 148(5), 529-544.
https://doi.org/10.1007/s00418-017-1590-4

Divac Rankov A, Ljujić M, Petrić M, Radojković D, Pesić M, Dinić J. Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology. 2017;148(5):529-544.
doi:10.1007/s00418-017-1590-4 .

Divac Rankov, Aleksandra, Ljujić, Mila, Petrić, Marija, Radojković, Dragica, Pesić, Milica, Dinić, Jelena, "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells" in Histochemistry and Cell Biology, 148, no. 5 (2017):529-544,
https://doi.org/10.1007/s00418-017-1590-4 . .

TY  - JOUR
AU  - Divac Rankov, Aleksandra
AU  - Ljujić, Mila
AU  - Petrić, Marija
AU  - Radojković, Dragica
AU  - Pesić, Milica
AU  - Dinić, Jelena
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1004
AB  - Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.
PB  - Springer, New York
T2  - Histochemistry and Cell Biology
T1  - Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells
EP  - 544
IS  - 5
SP  - 529
VL  - 148
DO  - 10.1007/s00418-017-1590-4
ER  - 

@article{
author = "Divac Rankov, Aleksandra and Ljujić, Mila and Petrić, Marija and Radojković, Dragica and Pesić, Milica and Dinić, Jelena",
year = "2017",
abstract = "Autophagy is linked to multiple cancer-related signaling pathways, and represents a defense mechanism for cancer cells under therapeutic stress. The crosstalk between apoptosis and autophagy is essential for both tumorigenesis and embryonic development. We studied the influence of autophagy on cell survival in pro-apoptotic conditions induced by anticancer drugs in three model systems: human cancer cells (NCI-H460, COR-L23 and U87), human normal cells (HaCaT and MRC-5) and zebrafish embryos (Danio rerio). Autophagy induction with AZD2014 and tamoxifen antagonized the pro-apoptotic effect of chemotherapeutics doxorubicin and cisplatin in cell lines, while autophagy inhibition by wortmannin and chloroquine synergized the action of both anticancer agents. This effect was further verified by assessing cleaved caspase-3 and PARP-1 levels. Autophagy inhibitors significantly increased both apoptotic markers when applied in combination with doxorubicin while autophagy inducers had the opposite effect. In a similar manner, autophagy induction in zebrafish embryos prevented cisplatin-induced apoptosis in the tail region while autophagy inhibition increased cell death in the tail and retina of cisplatin-treated animals. Autophagy modulation with direct inhibitors of the PI3kinase/Akt/mTOR pathway (AZD2014 and wortmannin) triggered the cellular response to anticancer drugs more effectively in NCI-H460 and zebrafish embryonic models compared to HaCaT suggesting that these modulators are selective towards rapidly proliferating cells. Therefore, evaluating the autophagic properties of chemotherapeutics could help determine more accurately the fate of different cell types under treatment. Our study underlines the importance of testing autophagic activity of potential anticancer agents in a comparative approach to develop more rational anticancer therapeutic strategies.",
publisher = "Springer, New York",
journal = "Histochemistry and Cell Biology",
title = "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells",
pages = "544-529",
number = "5",
volume = "148",
doi = "10.1007/s00418-017-1590-4"
}

Divac Rankov, A., Ljujić, M., Petrić, M., Radojković, D., Pesić, M.,& Dinić, J.. (2017). Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology
Springer, New York., 148(5), 529-544.
https://doi.org/10.1007/s00418-017-1590-4

Divac Rankov A, Ljujić M, Petrić M, Radojković D, Pesić M, Dinić J. Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells. in Histochemistry and Cell Biology. 2017;148(5):529-544.
doi:10.1007/s00418-017-1590-4 .

Divac Rankov, Aleksandra, Ljujić, Mila, Petrić, Marija, Radojković, Dragica, Pesić, Milica, Dinić, Jelena, "Targeting autophagy to modulate cell survival: a comparative analysis in cancer, normal and embryonic cells" in Histochemistry and Cell Biology, 148, no. 5 (2017):529-544,
https://doi.org/10.1007/s00418-017-1590-4 . .

TY  - JOUR
AU  - Ljujić, Mila
AU  - Mijatović, Sanja
AU  - Bulatović, Mirna Z.
AU  - Mojić, Marija
AU  - Maksimović-Ivanić, Danijela
AU  - Radojković, Dragica
AU  - Topić, Aleksandra
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1044
AB  - Increased circulating alpha-1-antitrypsin (AAT) correlates with cancer stage/aggressiveness, but its role in cancer biology is unclear. We revealed antagonistic effect of AAT to cisplatin-induced cytotoxicity in prostate (PC3) and melanoma (A375) cancer cell lines. Moreover, AAT abrogated cytotoxicity of MEK inhibitor U0126 in PC3 cell line. Weaker antagonistic effect of AAT on cytotoxicity of PI3/Akt and NF-kB inhibitors was also observed. In addition, cisplatin increased AAT gene expression in transfected PC3 cells. However, AAT derived from transfected PC3 cells did not antagonize cisplatin-induced cytotoxicity. In conclusion, these results suggest possible association between high circulating AAT and cisplatin resistance.
PB  - Springer, Dordrecht
T2  - Pathology & Oncology Research
T1  - Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines
EP  - 343
IS  - 2
SP  - 335
VL  - 23
DO  - 10.1007/s12253-016-0104-3
ER  - 

@article{
author = "Ljujić, Mila and Mijatović, Sanja and Bulatović, Mirna Z. and Mojić, Marija and Maksimović-Ivanić, Danijela and Radojković, Dragica and Topić, Aleksandra",
year = "2017",
abstract = "Increased circulating alpha-1-antitrypsin (AAT) correlates with cancer stage/aggressiveness, but its role in cancer biology is unclear. We revealed antagonistic effect of AAT to cisplatin-induced cytotoxicity in prostate (PC3) and melanoma (A375) cancer cell lines. Moreover, AAT abrogated cytotoxicity of MEK inhibitor U0126 in PC3 cell line. Weaker antagonistic effect of AAT on cytotoxicity of PI3/Akt and NF-kB inhibitors was also observed. In addition, cisplatin increased AAT gene expression in transfected PC3 cells. However, AAT derived from transfected PC3 cells did not antagonize cisplatin-induced cytotoxicity. In conclusion, these results suggest possible association between high circulating AAT and cisplatin resistance.",
publisher = "Springer, Dordrecht",
journal = "Pathology & Oncology Research",
title = "Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines",
pages = "343-335",
number = "2",
volume = "23",
doi = "10.1007/s12253-016-0104-3"
}

Ljujić, M., Mijatović, S., Bulatović, M. Z., Mojić, M., Maksimović-Ivanić, D., Radojković, D.,& Topić, A.. (2017). Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines. in Pathology & Oncology Research
Springer, Dordrecht., 23(2), 335-343.
https://doi.org/10.1007/s12253-016-0104-3

Ljujić M, Mijatović S, Bulatović MZ, Mojić M, Maksimović-Ivanić D, Radojković D, Topić A. Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines. in Pathology & Oncology Research. 2017;23(2):335-343.
doi:10.1007/s12253-016-0104-3 .

Ljujić, Mila, Mijatović, Sanja, Bulatović, Mirna Z., Mojić, Marija, Maksimović-Ivanić, Danijela, Radojković, Dragica, Topić, Aleksandra, "Alpha-1-Antitrypsin Antagonizes Cisplatin-Induced Cytotoxicity in Prostate Cancer (PC3) and Melanoma Cancer (A375) Cell Lines" in Pathology & Oncology Research, 23, no. 2 (2017):335-343,
https://doi.org/10.1007/s12253-016-0104-3 . .

TY  - JOUR
AU  - Pakos-Zebrucka, Karolina
AU  - Koryga, Izabela
AU  - Mnich, Katarzyna
AU  - Ljujić, Mila
AU  - Samali, Afshin
AU  - Gorman, Adrienne M.
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/927
AB  - In response to diverse stress stimuli, eukaryotic cells activate a common adaptive pathway, termed the integrated stress response (ISR), to restore cellular homeostasis. The core event in this pathway is the phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2 alpha) by one of four members of the eIF2 alpha kinase family, which leads to a decrease in global protein synthesis and the induction of selected genes, including the transcription factor ATF4, that together promote cellular recovery. The gene expression program activated by the ISR optimizes the cellular response to stress and is dependent on the cellular context, as well as on the nature and intensity of the stress stimuli. Although the ISR is primarily a pro-survival, homeostatic program, exposure to severe stress can drive signaling toward cell death. Here, we review current understanding of the ISR signaling and how it regulates cell fate under diverse types of stress.
PB  - Wiley, Hoboken
T2  - EMBO Reports
T1  - The integrated stress response
EP  - 1395
IS  - 10
SP  - 1374
VL  - 17
DO  - 10.15252/embr.201642195
ER  - 

@article{
author = "Pakos-Zebrucka, Karolina and Koryga, Izabela and Mnich, Katarzyna and Ljujić, Mila and Samali, Afshin and Gorman, Adrienne M.",
year = "2016",
abstract = "In response to diverse stress stimuli, eukaryotic cells activate a common adaptive pathway, termed the integrated stress response (ISR), to restore cellular homeostasis. The core event in this pathway is the phosphorylation of eukaryotic translation initiation factor 2 alpha (eIF2 alpha) by one of four members of the eIF2 alpha kinase family, which leads to a decrease in global protein synthesis and the induction of selected genes, including the transcription factor ATF4, that together promote cellular recovery. The gene expression program activated by the ISR optimizes the cellular response to stress and is dependent on the cellular context, as well as on the nature and intensity of the stress stimuli. Although the ISR is primarily a pro-survival, homeostatic program, exposure to severe stress can drive signaling toward cell death. Here, we review current understanding of the ISR signaling and how it regulates cell fate under diverse types of stress.",
publisher = "Wiley, Hoboken",
journal = "EMBO Reports",
title = "The integrated stress response",
pages = "1395-1374",
number = "10",
volume = "17",
doi = "10.15252/embr.201642195"
}

Pakos-Zebrucka, K., Koryga, I., Mnich, K., Ljujić, M., Samali, A.,& Gorman, A. M.. (2016). The integrated stress response. in EMBO Reports
Wiley, Hoboken., 17(10), 1374-1395.
https://doi.org/10.15252/embr.201642195

Pakos-Zebrucka K, Koryga I, Mnich K, Ljujić M, Samali A, Gorman AM. The integrated stress response. in EMBO Reports. 2016;17(10):1374-1395.
doi:10.15252/embr.201642195 .

Pakos-Zebrucka, Karolina, Koryga, Izabela, Mnich, Katarzyna, Ljujić, Mila, Samali, Afshin, Gorman, Adrienne M., "The integrated stress response" in EMBO Reports, 17, no. 10 (2016):1374-1395,
https://doi.org/10.15252/embr.201642195 . .

TY  - JOUR
AU  - Topić, Aleksandra
AU  - Nagorni-Obradović, Ljudmila
AU  - Francuski, Djordje
AU  - Ljujić, Mila
AU  - Malić, Zivka
AU  - Radojković, Dragica
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/900
AB  - Alpha-1-antitrypsin deficiency (AATD) and tobacco smoke play a key role in the pathogenesis of early-onset emphysema. Differences in AATD-related chronic obstructive pulmonary disease stages imply the existence of modifying factors associated with disease severity. We present two male patients with emphysema caused by severe AATD (PiZZ genotype). Both are former smokers and have epoxide hydrolase low-activity phenotype. Extremely high level of oxidative stress (high urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine), increased inflammation (high serum CRP), and GSTP1 105Val mutation were found in patient with a worse lung function and prognosis. These data provide more evidence that oxidative stress-related gene variants and inflammation are associated with worse symptoms of AATD-related emphysema. Therefore, prevention against severe stage of AATD-related emphysema would include early identification of the risk gene variants, cessation or never smoking, and treatment with anti-inflammatory and anti-oxidant drugs. Additionally, urinary 8-oxodG could be a candidate for predictive biomarker for routine assessment of the oxidative stress level in AATD patients.
PB  - Springer/Plenum Publishers, New York
T2  - Biochemical Genetics
T1  - Oxidative Stress and Polymorphism of Xenobiotic-Metabolizing Enzymes in Two Patients with Severe Alpha-1-Antitrypsin Deficiency
EP  - 752
IS  - 5
SP  - 746
VL  - 54
DO  - 10.1007/s10528-016-9748-7
ER  - 

@article{
author = "Topić, Aleksandra and Nagorni-Obradović, Ljudmila and Francuski, Djordje and Ljujić, Mila and Malić, Zivka and Radojković, Dragica",
year = "2016",
abstract = "Alpha-1-antitrypsin deficiency (AATD) and tobacco smoke play a key role in the pathogenesis of early-onset emphysema. Differences in AATD-related chronic obstructive pulmonary disease stages imply the existence of modifying factors associated with disease severity. We present two male patients with emphysema caused by severe AATD (PiZZ genotype). Both are former smokers and have epoxide hydrolase low-activity phenotype. Extremely high level of oxidative stress (high urinary 8-oxo-7,8-dihydro-2'-deoxyguanosine), increased inflammation (high serum CRP), and GSTP1 105Val mutation were found in patient with a worse lung function and prognosis. These data provide more evidence that oxidative stress-related gene variants and inflammation are associated with worse symptoms of AATD-related emphysema. Therefore, prevention against severe stage of AATD-related emphysema would include early identification of the risk gene variants, cessation or never smoking, and treatment with anti-inflammatory and anti-oxidant drugs. Additionally, urinary 8-oxodG could be a candidate for predictive biomarker for routine assessment of the oxidative stress level in AATD patients.",
publisher = "Springer/Plenum Publishers, New York",
journal = "Biochemical Genetics",
title = "Oxidative Stress and Polymorphism of Xenobiotic-Metabolizing Enzymes in Two Patients with Severe Alpha-1-Antitrypsin Deficiency",
pages = "752-746",
number = "5",
volume = "54",
doi = "10.1007/s10528-016-9748-7"
}

Topić, A., Nagorni-Obradović, L., Francuski, D., Ljujić, M., Malić, Z.,& Radojković, D.. (2016). Oxidative Stress and Polymorphism of Xenobiotic-Metabolizing Enzymes in Two Patients with Severe Alpha-1-Antitrypsin Deficiency. in Biochemical Genetics
Springer/Plenum Publishers, New York., 54(5), 746-752.
https://doi.org/10.1007/s10528-016-9748-7

Topić A, Nagorni-Obradović L, Francuski D, Ljujić M, Malić Z, Radojković D. Oxidative Stress and Polymorphism of Xenobiotic-Metabolizing Enzymes in Two Patients with Severe Alpha-1-Antitrypsin Deficiency. in Biochemical Genetics. 2016;54(5):746-752.
doi:10.1007/s10528-016-9748-7 .

Topić, Aleksandra, Nagorni-Obradović, Ljudmila, Francuski, Djordje, Ljujić, Mila, Malić, Zivka, Radojković, Dragica, "Oxidative Stress and Polymorphism of Xenobiotic-Metabolizing Enzymes in Two Patients with Severe Alpha-1-Antitrypsin Deficiency" in Biochemical Genetics, 54, no. 5 (2016):746-752,
https://doi.org/10.1007/s10528-016-9748-7 . .

TY  - JOUR
AU  - Klionsky, D.J.
AU  - Abdelmohsen, Kotb
AU  - Ljujić, Mila
AU  - Bumbasirević, V.
AU  - Deretić, V.
AU  - Dikić, I.
AU  - Glavić, A.
AU  - Harhaji-Trajković, L.
AU  - Isaković, A.J.
AU  - Kravić-Stevović, T.
AU  - Marković, I.
AU  - Polčić, Peter
AU  - Topisirović, I.
AU  - Trajković, V.
AU  - (broj koautora 2463)
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/970
PB  - Taylor and Francis Inc.
T2  - Autophagy
T1  - Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356
IS  - 2
SP  - 443
VL  - 12
DO  - 10.1080/15548627.2016.1147886
ER  - 

@article{
author = "Klionsky, D.J. and Abdelmohsen, Kotb and Ljujić, Mila and Bumbasirević, V. and Deretić, V. and Dikić, I. and Glavić, A. and Harhaji-Trajković, L. and Isaković, A.J. and Kravić-Stevović, T. and Marković, I. and Polčić, Peter and Topisirović, I. and Trajković, V. and (broj koautora 2463)",
year = "2016",
publisher = "Taylor and Francis Inc.",
journal = "Autophagy",
title = "Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356",
number = "2",
pages = "443",
volume = "12",
doi = "10.1080/15548627.2016.1147886"
}

Klionsky, D.J., Abdelmohsen, K., Ljujić, M., Bumbasirević, V., Deretić, V., Dikić, I., Glavić, A., Harhaji-Trajković, L., Isaković, A.J., Kravić-Stevović, T., Marković, I., Polčić, P., Topisirović, I., Trajković, V.,& (broj koautora 2463). (2016). Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356. in Autophagy
Taylor and Francis Inc.., 12(2), 443.
https://doi.org/10.1080/15548627.2016.1147886

Klionsky D, Abdelmohsen K, Ljujić M, Bumbasirević V, Deretić V, Dikić I, Glavić A, Harhaji-Trajković L, Isaković A, Kravić-Stevović T, Marković I, Polčić P, Topisirović I, Trajković V, (broj koautora 2463). Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356. in Autophagy. 2016;12(2):443.
doi:10.1080/15548627.2016.1147886 .

Klionsky, D.J., Abdelmohsen, Kotb, Ljujić, Mila, Bumbasirević, V., Deretić, V., Dikić, I., Glavić, A., Harhaji-Trajković, L., Isaković, A.J., Kravić-Stevović, T., Marković, I., Polčić, Peter, Topisirović, I., Trajković, V., (broj koautora 2463), "Erratum to: Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition) (Autophagy, 12, 1, 1-222, 10.1080/15548627.2015.1100356" in Autophagy, 12, no. 2 (2016):443,
https://doi.org/10.1080/15548627.2016.1147886 . .

TY  - JOUR
AU  - Klionsky, Daniel J.
AU  - Abdelmohsen, Kotb
AU  - Bumbasirević, Vladimir
AU  - Deretić, Vojo
AU  - Dikić, Ivan
AU  - Glavić, Alvaro
AU  - Harhaji-Trajković, Ljubica
AU  - Isaković, Aleksandra J.
AU  - Kravić-Stevović, Tamara
AU  - Ljujić, Mila
AU  - Marković, Ivanka
AU  - Polčić, Peter
AU  - Topisirović, Ivan
AU  - Trajković, Vladimir
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/985
PB  - Taylor & Francis Inc, Philadelphia
T2  - Autophagy
T1  - Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)
EP  - 222
IS  - 1
SP  - 1
VL  - 12
DO  - 10.1080/15548627.2015.1100356
ER  - 

@article{
author = "Klionsky, Daniel J. and Abdelmohsen, Kotb and Bumbasirević, Vladimir and Deretić, Vojo and Dikić, Ivan and Glavić, Alvaro and Harhaji-Trajković, Ljubica and Isaković, Aleksandra J. and Kravić-Stevović, Tamara and Ljujić, Mila and Marković, Ivanka and Polčić, Peter and Topisirović, Ivan and Trajković, Vladimir",
year = "2016",
publisher = "Taylor & Francis Inc, Philadelphia",
journal = "Autophagy",
title = "Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)",
pages = "222-1",
number = "1",
volume = "12",
doi = "10.1080/15548627.2015.1100356"
}

Klionsky, D. J., Abdelmohsen, K., Bumbasirević, V., Deretić, V., Dikić, I., Glavić, A., Harhaji-Trajković, L., Isaković, A. J., Kravić-Stevović, T., Ljujić, M., Marković, I., Polčić, P., Topisirović, I.,& Trajković, V.. (2016). Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). in Autophagy
Taylor & Francis Inc, Philadelphia., 12(1), 1-222.
https://doi.org/10.1080/15548627.2015.1100356

Klionsky DJ, Abdelmohsen K, Bumbasirević V, Deretić V, Dikić I, Glavić A, Harhaji-Trajković L, Isaković AJ, Kravić-Stevović T, Ljujić M, Marković I, Polčić P, Topisirović I, Trajković V. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). in Autophagy. 2016;12(1):1-222.
doi:10.1080/15548627.2015.1100356 .

Klionsky, Daniel J., Abdelmohsen, Kotb, Bumbasirević, Vladimir, Deretić, Vojo, Dikić, Ivan, Glavić, Alvaro, Harhaji-Trajković, Ljubica, Isaković, Aleksandra J., Kravić-Stevović, Tamara, Ljujić, Mila, Marković, Ivanka, Polčić, Peter, Topisirović, Ivan, Trajković, Vladimir, "Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition)" in Autophagy, 12, no. 1 (2016):1-222,
https://doi.org/10.1080/15548627.2015.1100356 . .