TY  - JOUR
AU  - Đedović, Neda
AU  - Jevtić, Bojan
AU  - Jose Mansilla, M.
AU  - Petković, Filip
AU  - Blazevski, Jana
AU  - Timotijević, Gordana
AU  - Navarro-Barriuso, Juan
AU  - Martinez-Caceres, Eva
AU  - Mostarica Stojkovide, Marija
AU  - Miljković, Đorđe
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1252
AB  - Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4(+) T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4(+) T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.
PB  - Elsevier Gmbh, Munich
T2  - Immunobiology
T1  - Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats
EP  - 476
IS  - 3
SP  - 470
VL  - 224
DO  - 10.1016/j.imbio.2019.01.001
ER  - 

@article{
author = "Đedović, Neda and Jevtić, Bojan and Jose Mansilla, M. and Petković, Filip and Blazevski, Jana and Timotijević, Gordana and Navarro-Barriuso, Juan and Martinez-Caceres, Eva and Mostarica Stojkovide, Marija and Miljković, Đorđe",
year = "2019",
abstract = "Dendritic cells (DC) are responsible for the initiation and shaping of the adaptive immune response and are in the focus of autoimmunity research. We were interested in comparison of DC obtained from autoimmunity-prone Dark Agouti (DA) rats and autoimmunity-resistant Albino Oxford (AO) rats. DC were generated from bone marrow precursors and matured (mDC) by lipopolysaccharide. Tolerogenic DC (tolDC) obtained by vitamin D3 treatment were studied in parallel. Profile of cytokine production was different in AO and DA mDC and tolDC. Expression of MHC class II molecules and CD86 were higher in DA DC, while vitamin D3 reduced their expression in dendritic cells of both strains. Allogeneic proliferation of CD4(+) T cells was reduced by AO tolDC, but not with DA tolDC in comparison to respective mDC. Finally, expression of various genes identified as differentially expressed in human mDC and tolDC was also analyzed in AO and DA DC. Again, AO and DA DC differed in the expression of the analyzed genes. To conclude, AO and DA DC differ in production of cytokines, expression of antigen presentation-related molecules and in regulation of CD4(+) T proliferation. The difference is valuable for understanding the divergence of the strains in their susceptibility to autoimmunity.",
publisher = "Elsevier Gmbh, Munich",
journal = "Immunobiology",
title = "Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats",
pages = "476-470",
number = "3",
volume = "224",
doi = "10.1016/j.imbio.2019.01.001"
}

Đedović, N., Jevtić, B., Jose Mansilla, M., Petković, F., Blazevski, J., Timotijević, G., Navarro-Barriuso, J., Martinez-Caceres, E., Mostarica Stojkovide, M.,& Miljković, Đ.. (2019). Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats. in Immunobiology
Elsevier Gmbh, Munich., 224(3), 470-476.
https://doi.org/10.1016/j.imbio.2019.01.001

Đedović N, Jevtić B, Jose Mansilla M, Petković F, Blazevski J, Timotijević G, Navarro-Barriuso J, Martinez-Caceres E, Mostarica Stojkovide M, Miljković Đ. Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats. in Immunobiology. 2019;224(3):470-476.
doi:10.1016/j.imbio.2019.01.001 .

Đedović, Neda, Jevtić, Bojan, Jose Mansilla, M., Petković, Filip, Blazevski, Jana, Timotijević, Gordana, Navarro-Barriuso, Juan, Martinez-Caceres, Eva, Mostarica Stojkovide, Marija, Miljković, Đorđe, "Comparison of dendritic cells obtained from autoimmunty-prone and resistant rats" in Immunobiology, 224, no. 3 (2019):470-476,
https://doi.org/10.1016/j.imbio.2019.01.001 . .

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Cepić, Aleksa
AU  - Bojić, Svetlana
AU  - Veljović, Katarina
AU  - Mihajlović, Sanja
AU  - Dedović, Neda
AU  - Jevtić, Bojan
AU  - Momcilović, Miljana
AU  - Lazarević, Milica
AU  - Mostarica-Stojković, Marija
AU  - Miljković, Đorđe
AU  - Golić, Nataša
PY  - 2019
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1272
AB  - Gut microbiota dysbiosis has been considered the essential element in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Antibiotics were administered orally to Dark Agouti (DA) rats early in their life with the aim of perturbing gut microbiota and investigating the effects of such intervention on the course of EAE. As a result, the diversity of the gut microbiota was reduced under the influence of antibiotics. Mainly, Firmicutes and Actinobacteria were replaced by Proteobacteria and Bacteroidetes, while decreased proportions of Clostridia and Bacilli classes were accompanied by an increase in Gamma-Proteobacteria in antibiotic-treated animals. Interestingly, a notable decrease in the Helicobacteraceae, Spirochaetaceae and Turicibacteriaceae was scored in antibiotic-treated groups. Also, levels of short chain fatty acids were reduced in the faeces of antibiotic-treated rats. Consequently, aggravation of EAE, paralleled with stronger immune response in lymph nodes draining the site of immunization, and increased inflammation within the CNS, were observed in antibiotic-treated DA rats. Thus, the alteration of gut microbiota leads to an escalation of CNS-directed autoimmunity in DA rats. The results of this study indicate that antibiotic use in early life may have subsequent unfavourable effects on the regulation of the immune system.
PB  - Nature Publishing Group, London
T2  - Scientific Reports
T1  - Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats
SP  - 918
VL  - 9
DO  - 10.1038/s41598-018-37505-7
ER  - 

@article{
author = "Stanisavljević, Suzana and Cepić, Aleksa and Bojić, Svetlana and Veljović, Katarina and Mihajlović, Sanja and Dedović, Neda and Jevtić, Bojan and Momcilović, Miljana and Lazarević, Milica and Mostarica-Stojković, Marija and Miljković, Đorđe and Golić, Nataša",
year = "2019",
abstract = "Gut microbiota dysbiosis has been considered the essential element in the pathogenesis of multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis (EAE). Antibiotics were administered orally to Dark Agouti (DA) rats early in their life with the aim of perturbing gut microbiota and investigating the effects of such intervention on the course of EAE. As a result, the diversity of the gut microbiota was reduced under the influence of antibiotics. Mainly, Firmicutes and Actinobacteria were replaced by Proteobacteria and Bacteroidetes, while decreased proportions of Clostridia and Bacilli classes were accompanied by an increase in Gamma-Proteobacteria in antibiotic-treated animals. Interestingly, a notable decrease in the Helicobacteraceae, Spirochaetaceae and Turicibacteriaceae was scored in antibiotic-treated groups. Also, levels of short chain fatty acids were reduced in the faeces of antibiotic-treated rats. Consequently, aggravation of EAE, paralleled with stronger immune response in lymph nodes draining the site of immunization, and increased inflammation within the CNS, were observed in antibiotic-treated DA rats. Thus, the alteration of gut microbiota leads to an escalation of CNS-directed autoimmunity in DA rats. The results of this study indicate that antibiotic use in early life may have subsequent unfavourable effects on the regulation of the immune system.",
publisher = "Nature Publishing Group, London",
journal = "Scientific Reports",
title = "Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats",
pages = "918",
volume = "9",
doi = "10.1038/s41598-018-37505-7"
}

Stanisavljević, S., Cepić, A., Bojić, S., Veljović, K., Mihajlović, S., Dedović, N., Jevtić, B., Momcilović, M., Lazarević, M., Mostarica-Stojković, M., Miljković, Đ.,& Golić, N.. (2019). Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats. in Scientific Reports
Nature Publishing Group, London., 9, 918.
https://doi.org/10.1038/s41598-018-37505-7

Stanisavljević S, Cepić A, Bojić S, Veljović K, Mihajlović S, Dedović N, Jevtić B, Momcilović M, Lazarević M, Mostarica-Stojković M, Miljković Đ, Golić N. Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats. in Scientific Reports. 2019;9:918.
doi:10.1038/s41598-018-37505-7 .

Stanisavljević, Suzana, Cepić, Aleksa, Bojić, Svetlana, Veljović, Katarina, Mihajlović, Sanja, Dedović, Neda, Jevtić, Bojan, Momcilović, Miljana, Lazarević, Milica, Mostarica-Stojković, Marija, Miljković, Đorđe, Golić, Nataša, "Oral neonatal antibiotic treatment perturbs gut microbiota and aggravates central nervous system autoimmunity in Dark Agouti rats" in Scientific Reports, 9 (2019):918,
https://doi.org/10.1038/s41598-018-37505-7 . .

TY  - JOUR
AU  - Vujicić, Milica
AU  - Saksida, Tamara
AU  - Despotović, Sanja
AU  - Soković Bajić, Svetlana
AU  - Lalić, Ivana
AU  - Koprivica, Ivan
AU  - Gajić, Dragica
AU  - Golić, Nataša
AU  - Tolinački, Maja
AU  - Stojanović, Ivana
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1182
AB  - Macrophage migration inhibitory factor (MIF) is a multifunctional protein that is involved in the development of gut-related inflammation. To investigate the role of MIF in the function of the intestinal barrier, we have explored intestinal permeability and gut-associated immune response in MIF-deficient (MIF-KO) mice. The absence of MIF provoked impairment of tight and adherens epithelial junctions in the colon through the disturbance of E-cadherin, zonula occludens-1, occludin and claudin-2 expression, which lead to the increase of intestinal barrier permeability. In these circumstances the diversity and content of gut microbiota in MIF-KO mice was considerably different compared to wild type mice. This change in microbiota was accompanied by an increased intestinal IgA concentration and a higher production of pro-inflammatory cytokines TNF and IFN-gamma in mesenteric lymph nodes of MIF-KO mice. The forced changes of microbiota executed by antibiotics prevented the "leakage" of the barrier in MIF-KO mice, probably through up-regulation of occludin expression and normalization of cellular pore diameters. In addition, cytokine secretion was normalized after the treatment with antibiotics. These results suggest that MIF participates in the maintenance of physiological microbiota diversity and immunosurveillance, which in turn enables the proper intestinal barrier function.
PB  - Nature Publishing Group, London
T2  - Scientific Reports
T1  - The Role of Macrophage Migration Inhibitory Factor in the Function of Intestinal Barrier
VL  - 8
DO  - 10.1038/s41598-018-24706-3
ER  - 

@article{
author = "Vujicić, Milica and Saksida, Tamara and Despotović, Sanja and Soković Bajić, Svetlana and Lalić, Ivana and Koprivica, Ivan and Gajić, Dragica and Golić, Nataša and Tolinački, Maja and Stojanović, Ivana",
year = "2018",
abstract = "Macrophage migration inhibitory factor (MIF) is a multifunctional protein that is involved in the development of gut-related inflammation. To investigate the role of MIF in the function of the intestinal barrier, we have explored intestinal permeability and gut-associated immune response in MIF-deficient (MIF-KO) mice. The absence of MIF provoked impairment of tight and adherens epithelial junctions in the colon through the disturbance of E-cadherin, zonula occludens-1, occludin and claudin-2 expression, which lead to the increase of intestinal barrier permeability. In these circumstances the diversity and content of gut microbiota in MIF-KO mice was considerably different compared to wild type mice. This change in microbiota was accompanied by an increased intestinal IgA concentration and a higher production of pro-inflammatory cytokines TNF and IFN-gamma in mesenteric lymph nodes of MIF-KO mice. The forced changes of microbiota executed by antibiotics prevented the "leakage" of the barrier in MIF-KO mice, probably through up-regulation of occludin expression and normalization of cellular pore diameters. In addition, cytokine secretion was normalized after the treatment with antibiotics. These results suggest that MIF participates in the maintenance of physiological microbiota diversity and immunosurveillance, which in turn enables the proper intestinal barrier function.",
publisher = "Nature Publishing Group, London",
journal = "Scientific Reports",
title = "The Role of Macrophage Migration Inhibitory Factor in the Function of Intestinal Barrier",
volume = "8",
doi = "10.1038/s41598-018-24706-3"
}

Vujicić, M., Saksida, T., Despotović, S., Soković Bajić, S., Lalić, I., Koprivica, I., Gajić, D., Golić, N., Tolinački, M.,& Stojanović, I.. (2018). The Role of Macrophage Migration Inhibitory Factor in the Function of Intestinal Barrier. in Scientific Reports
Nature Publishing Group, London., 8.
https://doi.org/10.1038/s41598-018-24706-3

Vujicić M, Saksida T, Despotović S, Soković Bajić S, Lalić I, Koprivica I, Gajić D, Golić N, Tolinački M, Stojanović I. The Role of Macrophage Migration Inhibitory Factor in the Function of Intestinal Barrier. in Scientific Reports. 2018;8.
doi:10.1038/s41598-018-24706-3 .

Vujicić, Milica, Saksida, Tamara, Despotović, Sanja, Soković Bajić, Svetlana, Lalić, Ivana, Koprivica, Ivan, Gajić, Dragica, Golić, Nataša, Tolinački, Maja, Stojanović, Ivana, "The Role of Macrophage Migration Inhibitory Factor in the Function of Intestinal Barrier" in Scientific Reports, 8 (2018),
https://doi.org/10.1038/s41598-018-24706-3 . .

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Dinić, Miroslav
AU  - Jevtić, Bojan
AU  - Dedović, Neda
AU  - Momcilović, Miljana
AU  - Đokić, Jelena
AU  - Golić, Nataša
AU  - Mostarica-Stojković, Marija
AU  - Miljković, Đorđe
PY  - 2018
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1179
AB  - Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-. and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Immunology
T1  - Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis
VL  - 9
DO  - 10.3389/fimmu.2018.00942
ER  - 

@article{
author = "Stanisavljević, Suzana and Dinić, Miroslav and Jevtić, Bojan and Dedović, Neda and Momcilović, Miljana and Đokić, Jelena and Golić, Nataša and Mostarica-Stojković, Marija and Miljković, Đorđe",
year = "2018",
abstract = "Albino Oxford (AO) rats are extremely resistant to induction of experimental autoimmune encephalomyelitis (EAE). EAE is an animal model of multiple sclerosis, a chronic inflammatory disease of the central nervous system (CNS), with established autoimmune pathogenesis. The autoimmune response against the antigens of the CNS is initiated in the peripheral lymphoid tissues after immunization of AO rats with CNS antigens. Subsequently, limited infiltration of the CNS occurs, yet without clinical sequels. It has recently become increasingly appreciated that gut-associated lymphoid tissues (GALT) and gut microbiota play an important role in regulation and propagation of encephalitogenic immune response. Therefore, modulation of AO gut microbiota by antibiotics was performed in this study. The treatment altered composition of gut microbiota in AO rats and led to a reduction in the proportion of regulatory T cells in Peyer's patches, mesenteric lymph nodes, and in lymph nodes draining the site of immunization. Upregulation of interferon-. and interleukin (IL)-17 production was observed in the draining lymph nodes. The treatment led to clinically manifested EAE in AO rats with more numerous infiltrates and higher production of IL-17 observed in the CNS. Importantly, transfer of AO gut microbiota into EAE-prone Dark Agouti rats ameliorated the disease. These results clearly imply that gut microbiota is an important factor in AO rat resistance to EAE and that gut microbiota transfer is an efficacious way to treat CNS autoimmunity. These findings also support the idea that gut microbiota modulation has a potential as a future treatment of multiple sclerosis.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Immunology",
title = "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis",
volume = "9",
doi = "10.3389/fimmu.2018.00942"
}

Stanisavljević, S., Dinić, M., Jevtić, B., Dedović, N., Momcilović, M., Đokić, J., Golić, N., Mostarica-Stojković, M.,& Miljković, Đ.. (2018). Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis. in Frontiers in Immunology
Frontiers Media Sa, Lausanne., 9.
https://doi.org/10.3389/fimmu.2018.00942

Stanisavljević S, Dinić M, Jevtić B, Dedović N, Momcilović M, Đokić J, Golić N, Mostarica-Stojković M, Miljković Đ. Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis. in Frontiers in Immunology. 2018;9.
doi:10.3389/fimmu.2018.00942 .

Stanisavljević, Suzana, Dinić, Miroslav, Jevtić, Bojan, Dedović, Neda, Momcilović, Miljana, Đokić, Jelena, Golić, Nataša, Mostarica-Stojković, Marija, Miljković, Đorđe, "Gut Microbiota Confers Resistance of Albino Oxford Rats to the Induction of Experimental Autoimmune Encephalomyelitis" in Frontiers in Immunology, 9 (2018),
https://doi.org/10.3389/fimmu.2018.00942 . .

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  - Jevtić, Bojan
AU  - Đedović, Neda
AU  - Stanisavljević, Suzana
AU  - Gašić, Uroš
AU  - Misić, Danijela
AU  - Despotović, Jovana
AU  - Samardžić, Jelena
AU  - Miljković, Djordje
AU  - Timotijević, Gordana
PY  - 2017
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/1000
AB  - Cucumber (Cucumis sativus) fruit has been used in cuisine worldwide, while its leaves are rich in immunomodulatory compounds. Cucumber leaf extract (CLE) was characterized by the predominance of triterpenoids cucurbitacins and significant levels of phenolics. Effects of CLE on CD4(+) T helper (Th) cells and macrophages, as the major encephalitogenic cells in the autoimmunity of the central nervous system were investigated in our study. CLE potently inhibited production of major pathogenic Th cytokines: interferon-gamma and interleukin-17, as well as of nitric oxide and reactive oxygen species in macrophages. Antigen-presenting activity of macrophages and dendritic cells was also affected by CLE. The effects of CLE were co-incident with modulation of NFKB and p38 MAPK signaling. Concentrations of CLE used in vitro did not show toxic effects on zebrafish embryos. Moreover, CLE inhibited generation of encephalitogenic cells in vivo. These results demonstrate that CLE deserve further investigation on its anti-encephalitogenic therapeutic properties.
PB  - Elsevier Science Bv, Amsterdam
T2  - Journal of Functional Foods
T1  - Anti-encephalitogenic effects of cucumber leaf extract
EP  - 262
SP  - 249
VL  - 37
DO  - 10.1016/j.jff.2017.07.060
ER  - 

@article{
author = "Jevtić, Bojan and Đedović, Neda and Stanisavljević, Suzana and Gašić, Uroš and Misić, Danijela and Despotović, Jovana and Samardžić, Jelena and Miljković, Djordje and Timotijević, Gordana",
year = "2017",
abstract = "Cucumber (Cucumis sativus) fruit has been used in cuisine worldwide, while its leaves are rich in immunomodulatory compounds. Cucumber leaf extract (CLE) was characterized by the predominance of triterpenoids cucurbitacins and significant levels of phenolics. Effects of CLE on CD4(+) T helper (Th) cells and macrophages, as the major encephalitogenic cells in the autoimmunity of the central nervous system were investigated in our study. CLE potently inhibited production of major pathogenic Th cytokines: interferon-gamma and interleukin-17, as well as of nitric oxide and reactive oxygen species in macrophages. Antigen-presenting activity of macrophages and dendritic cells was also affected by CLE. The effects of CLE were co-incident with modulation of NFKB and p38 MAPK signaling. Concentrations of CLE used in vitro did not show toxic effects on zebrafish embryos. Moreover, CLE inhibited generation of encephalitogenic cells in vivo. These results demonstrate that CLE deserve further investigation on its anti-encephalitogenic therapeutic properties.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Journal of Functional Foods",
title = "Anti-encephalitogenic effects of cucumber leaf extract",
pages = "262-249",
volume = "37",
doi = "10.1016/j.jff.2017.07.060"
}

Jevtić, B., Đedović, N., Stanisavljević, S., Gašić, U., Misić, D., Despotović, J., Samardžić, J., Miljković, D.,& Timotijević, G.. (2017). Anti-encephalitogenic effects of cucumber leaf extract. in Journal of Functional Foods
Elsevier Science Bv, Amsterdam., 37, 249-262.
https://doi.org/10.1016/j.jff.2017.07.060

Jevtić B, Đedović N, Stanisavljević S, Gašić U, Misić D, Despotović J, Samardžić J, Miljković D, Timotijević G. Anti-encephalitogenic effects of cucumber leaf extract. in Journal of Functional Foods. 2017;37:249-262.
doi:10.1016/j.jff.2017.07.060 .

Jevtić, Bojan, Đedović, Neda, Stanisavljević, Suzana, Gašić, Uroš, Misić, Danijela, Despotović, Jovana, Samardžić, Jelena, Miljković, Djordje, Timotijević, Gordana, "Anti-encephalitogenic effects of cucumber leaf extract" in Journal of Functional Foods, 37 (2017):249-262,
https://doi.org/10.1016/j.jff.2017.07.060 . .

TY  - JOUR
AU  - Stanisavljević, S.
AU  - Lukić, Jovanka
AU  - Momcilović, M.
AU  - Miljković, M.
AU  - Jevtić, B.
AU  - Kojić, Milan
AU  - Golić, Nataša
AU  - Mostarica Stojković, M.
AU  - Miljković, D.
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/947
AB  - Gut microbiota and gut-associated lymphoid tissue have been increasingly appreciated as important players in pathogenesis of various autoimmune diseases, including multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis that can be induced with an injection of spinal cord homogenate emulsified in complete Freund's adjuvant in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats. In this study, mesenteric lymph nodes (MLN), Peyer's patches (PP) and gut microbiota were analysed in these two rat strains. There was higher proportion of CD4(+) T cells and regulatory T cells in non-immunised DA rats in comparison to AO rats. Also, DA rat MLN and PP cells were higher producers of pro-inflammatory cytokines interferon-gamma and interleukin-17. Finally, microbial analyses showed that uncultivated species of Turicibacter and Atopostipes genus were exclusively present in AO rats, in faeces and intestinal tissue, respectively. Thus, it is clear that in comparison of an EAE-susceptible with an EAE-resistant strain of rats, various discrepancies at the level of gut associated lymphoid tissue, as well as at the level of gut microbiota can be observed. Future studies should determine if the differences have functional significance for EAE pathogenesis.
PB  - Wageningen Academic Publishers, Wageningen
T2  - Beneficial Microbes
T1  - Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis
EP  - 373
IS  - 3
SP  - 363
VL  - 7
DO  - 10.3920/BM2015.0159
ER  - 

@article{
author = "Stanisavljević, S. and Lukić, Jovanka and Momcilović, M. and Miljković, M. and Jevtić, B. and Kojić, Milan and Golić, Nataša and Mostarica Stojković, M. and Miljković, D.",
year = "2016",
abstract = "Gut microbiota and gut-associated lymphoid tissue have been increasingly appreciated as important players in pathogenesis of various autoimmune diseases, including multiple sclerosis. Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis that can be induced with an injection of spinal cord homogenate emulsified in complete Freund's adjuvant in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats. In this study, mesenteric lymph nodes (MLN), Peyer's patches (PP) and gut microbiota were analysed in these two rat strains. There was higher proportion of CD4(+) T cells and regulatory T cells in non-immunised DA rats in comparison to AO rats. Also, DA rat MLN and PP cells were higher producers of pro-inflammatory cytokines interferon-gamma and interleukin-17. Finally, microbial analyses showed that uncultivated species of Turicibacter and Atopostipes genus were exclusively present in AO rats, in faeces and intestinal tissue, respectively. Thus, it is clear that in comparison of an EAE-susceptible with an EAE-resistant strain of rats, various discrepancies at the level of gut associated lymphoid tissue, as well as at the level of gut microbiota can be observed. Future studies should determine if the differences have functional significance for EAE pathogenesis.",
publisher = "Wageningen Academic Publishers, Wageningen",
journal = "Beneficial Microbes",
title = "Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis",
pages = "373-363",
number = "3",
volume = "7",
doi = "10.3920/BM2015.0159"
}

Stanisavljević, S., Lukić, J., Momcilović, M., Miljković, M., Jevtić, B., Kojić, M., Golić, N., Mostarica Stojković, M.,& Miljković, D.. (2016). Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis. in Beneficial Microbes
Wageningen Academic Publishers, Wageningen., 7(3), 363-373.
https://doi.org/10.3920/BM2015.0159

Stanisavljević S, Lukić J, Momcilović M, Miljković M, Jevtić B, Kojić M, Golić N, Mostarica Stojković M, Miljković D. Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis. in Beneficial Microbes. 2016;7(3):363-373.
doi:10.3920/BM2015.0159 .

Stanisavljević, S., Lukić, Jovanka, Momcilović, M., Miljković, M., Jevtić, B., Kojić, Milan, Golić, Nataša, Mostarica Stojković, M., Miljković, D., "Gut-associated lymphoid tissue, gut microbes and susceptibility to experimental autoimmune encephalomyelitis" in Beneficial Microbes, 7, no. 3 (2016):363-373,
https://doi.org/10.3920/BM2015.0159 . .

TY  - JOUR
AU  - Stanisavljević, Suzana
AU  - Lukić, Jovanka
AU  - Soković Bajić, Svetlana
AU  - Mihajlović, Sanja
AU  - Mostarica Stojković, Marija
AU  - Miljković, Djordje
AU  - Golić, Nataša
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/950
AB  - Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It is widely accepted that autoimmune response against the antigens of the CNS is the essential pathogenic force in the disease. It has recently become increasingly appreciated that activated encephalitogenic cells tend to migrate toward gut associated lymphoid tissues (GALTs) and that interrupted balance between regulatory and inflammatory immunity within the GALT might have decisive role in the initiation and propagation of the CNS autoimmunity. Gut microbiota composition and function has the major impact on the balance in the GALT. Thus, our aim was to perform analyses of gut microbiota in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Albino Oxford (AO) rats that are highly resistant to EAE induction and Dark Agouti (DA) rats that develop EAE after mild immunization were compared for gut microbiota composition in different phases after EAE induction. Microbial analyses of the genus Lactobacillus and related lactic acid bacteria showed higher diversity of Lactobacillus spp. in EAE-resistant AO rats, while some members of Firmicutes and Proteobactene (Undibacterium oligocarboniphilum) were detected only in feces of DA rats at the peak of the disease (between 13 and 16 days after induction). Interestingly, in contrast to our previous study where Turicibacter sp. was found exclusively in non immunized AO, but not in DA rats, in this study it was detected in DA rats that remained healthy 16 days after induction, as well as in four of 12 DA rats at the peak of the disease. Similar observation was obtained for the members of Lachnospiraceae. Further, production of a typical regulatory cytokine interleukin-10 was compared in GALT cells of AO and DA rats, and higher production was observed in DA rats. Our data contribute to the idea that gut microbiota and GALT considerably influence multiple sclerosis pathogenesis.
PB  - Frontiers Media Sa, Lausanne
T2  - Frontiers in Microbiology
T1  - Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats
VL  - 7
DO  - 10.3389/fmicb.2016.02005
ER  - 

@article{
author = "Stanisavljević, Suzana and Lukić, Jovanka and Soković Bajić, Svetlana and Mihajlović, Sanja and Mostarica Stojković, Marija and Miljković, Djordje and Golić, Nataša",
year = "2016",
abstract = "Multiple sclerosis is a chronic inflammatory disease of the central nervous system (CNS). It is widely accepted that autoimmune response against the antigens of the CNS is the essential pathogenic force in the disease. It has recently become increasingly appreciated that activated encephalitogenic cells tend to migrate toward gut associated lymphoid tissues (GALTs) and that interrupted balance between regulatory and inflammatory immunity within the GALT might have decisive role in the initiation and propagation of the CNS autoimmunity. Gut microbiota composition and function has the major impact on the balance in the GALT. Thus, our aim was to perform analyses of gut microbiota in experimental autoimmune encephalomyelitis (EAE), an animal model of multiple sclerosis. Albino Oxford (AO) rats that are highly resistant to EAE induction and Dark Agouti (DA) rats that develop EAE after mild immunization were compared for gut microbiota composition in different phases after EAE induction. Microbial analyses of the genus Lactobacillus and related lactic acid bacteria showed higher diversity of Lactobacillus spp. in EAE-resistant AO rats, while some members of Firmicutes and Proteobactene (Undibacterium oligocarboniphilum) were detected only in feces of DA rats at the peak of the disease (between 13 and 16 days after induction). Interestingly, in contrast to our previous study where Turicibacter sp. was found exclusively in non immunized AO, but not in DA rats, in this study it was detected in DA rats that remained healthy 16 days after induction, as well as in four of 12 DA rats at the peak of the disease. Similar observation was obtained for the members of Lachnospiraceae. Further, production of a typical regulatory cytokine interleukin-10 was compared in GALT cells of AO and DA rats, and higher production was observed in DA rats. Our data contribute to the idea that gut microbiota and GALT considerably influence multiple sclerosis pathogenesis.",
publisher = "Frontiers Media Sa, Lausanne",
journal = "Frontiers in Microbiology",
title = "Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats",
volume = "7",
doi = "10.3389/fmicb.2016.02005"
}

Stanisavljević, S., Lukić, J., Soković Bajić, S., Mihajlović, S., Mostarica Stojković, M., Miljković, D.,& Golić, N.. (2016). Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats. in Frontiers in Microbiology
Frontiers Media Sa, Lausanne., 7.
https://doi.org/10.3389/fmicb.2016.02005

Stanisavljević S, Lukić J, Soković Bajić S, Mihajlović S, Mostarica Stojković M, Miljković D, Golić N. Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats. in Frontiers in Microbiology. 2016;7.
doi:10.3389/fmicb.2016.02005 .

Stanisavljević, Suzana, Lukić, Jovanka, Soković Bajić, Svetlana, Mihajlović, Sanja, Mostarica Stojković, Marija, Miljković, Djordje, Golić, Nataša, "Correlation of Gut Microbiota Composition with Resistance to Experimental Autoimmune Encephalomyelitis in Rats" in Frontiers in Microbiology, 7 (2016),
https://doi.org/10.3389/fmicb.2016.02005 . .

TY  - JOUR
AU  - Ljujić, Mila
AU  - Mijatović, S.
AU  - Bulatović, M. Z.
AU  - Mojić, M.
AU  - Maksimović-Ivanić, Danijela
AU  - Radojković, Dragica
AU  - Topić, Aleksandra
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/949
AB  - Alpha-1-antitrypsin (AAT), an acute phase protein, is the principal circulatory anti-protease. This multifunctional protein is encoded by the SERPINA1 gene. Although AAT was recognised as a potential tumour marker, its role in cancer biology remains unknown. Given that it has been demonstrated that AAT has an anti-apoptotic property against non-malignant cells, we aimed to investigate whether AAT affects apoptosis in a colon cancer cell line (HCT116). The presence of AAT in the HCT116 cell culture antagonized cytotoxicity of blockers of MEK1/2, PI3K/Akt pathways as well as NF-kappa B. The dominantly recovered cell viability was observed in the co-treatment with MEK1/2 inhibitor U0126. In addition, it was revealed that AAT almost completely abolished U0126-induced apoptosis through maintenance of the autophagy process. Our study revealed for the first time that the observed cyto-protection triggered by AAT was accompanied by sustained autophagy which opposed apoptosis. These results may contribute to understanding of the role of AAT in cancer development and evaluation of efficacy of cancer therapy.
PB  - Maik Nauka/Interperiodica/Springer, New York
T2  - Molecular Biology
T1  - ALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116)
EP  - 156
IS  - 1
SP  - 153
VL  - 50
DO  - 10.1134/S002689331601012X
ER  - 

@article{
author = "Ljujić, Mila and Mijatović, S. and Bulatović, M. Z. and Mojić, M. and Maksimović-Ivanić, Danijela and Radojković, Dragica and Topić, Aleksandra",
year = "2016",
abstract = "Alpha-1-antitrypsin (AAT), an acute phase protein, is the principal circulatory anti-protease. This multifunctional protein is encoded by the SERPINA1 gene. Although AAT was recognised as a potential tumour marker, its role in cancer biology remains unknown. Given that it has been demonstrated that AAT has an anti-apoptotic property against non-malignant cells, we aimed to investigate whether AAT affects apoptosis in a colon cancer cell line (HCT116). The presence of AAT in the HCT116 cell culture antagonized cytotoxicity of blockers of MEK1/2, PI3K/Akt pathways as well as NF-kappa B. The dominantly recovered cell viability was observed in the co-treatment with MEK1/2 inhibitor U0126. In addition, it was revealed that AAT almost completely abolished U0126-induced apoptosis through maintenance of the autophagy process. Our study revealed for the first time that the observed cyto-protection triggered by AAT was accompanied by sustained autophagy which opposed apoptosis. These results may contribute to understanding of the role of AAT in cancer development and evaluation of efficacy of cancer therapy.",
publisher = "Maik Nauka/Interperiodica/Springer, New York",
journal = "Molecular Biology",
title = "ALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116)",
pages = "156-153",
number = "1",
volume = "50",
doi = "10.1134/S002689331601012X"
}

Ljujić, M., Mijatović, S., Bulatović, M. Z., Mojić, M., Maksimović-Ivanić, D., Radojković, D.,& Topić, A.. (2016). ALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116). in Molecular Biology
Maik Nauka/Interperiodica/Springer, New York., 50(1), 153-156.
https://doi.org/10.1134/S002689331601012X

Ljujić M, Mijatović S, Bulatović MZ, Mojić M, Maksimović-Ivanić D, Radojković D, Topić A. ALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116). in Molecular Biology. 2016;50(1):153-156.
doi:10.1134/S002689331601012X .

Ljujić, Mila, Mijatović, S., Bulatović, M. Z., Mojić, M., Maksimović-Ivanić, Danijela, Radojković, Dragica, Topić, Aleksandra, "ALPHA-1 Antitrypsin Affects U0126-Induced Cytotoxicity in Colon Cancer Cell Line (HCT116)" in Molecular Biology, 50, no. 1 (2016):153-156,
https://doi.org/10.1134/S002689331601012X . .

TY  - JOUR
AU  - Jevtić, Bojan
AU  - Đedović, Neda
AU  - Stanisavljević, Suzana
AU  - Despotović, Jovana
AU  - Mijković, Djordje
AU  - Timotijević, Gordana
PY  - 2016
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/938
AB  - Cucurbitacin E (CucE) is a highly oxidized steroid consisting of a tetracyclic triterpene. It is a member of a Cucurbitacin family of biomolecules that are predominantly found in Cucurbitaceae plants. CucE has already been identified as a potent anti-inflammatory compound. Here, its effects on CD4(+) T helper (Th) cells and macrophages, as the major encephalitogenic cells in the autoimmunity of the central nervous system, were investigated. Production of major pathogenic Th cell cytokines: interferon-gamma and interleukin-17 were inhibited under the influence of CucE. The effects of CucE on CD4+ T cells were mediated through the modulation of aryl hydrocarbon receptor, STAT3, Na kappa B, p38 MAPK, and miR-146 signaling. Further, production of nitric oxide and reactive oxygen species, as well as phagocytic ability, were inhibited in macrophages treated with CucE. These results imply that CucE possesses powerful antiencephalitogenic activity.
PB  - Amer Chemical Soc, Washington
T2  - Journal of Agricultural and Food Chemistry
T1  - Cucurbitacin E Potently Modulates the Activity of Encephalitogenic Cells
EP  - 4907
IS  - 24
SP  - 4900
VL  - 64
DO  - 10.1021/acs.jafc.6b00951
ER  - 

@article{
author = "Jevtić, Bojan and Đedović, Neda and Stanisavljević, Suzana and Despotović, Jovana and Mijković, Djordje and Timotijević, Gordana",
year = "2016",
abstract = "Cucurbitacin E (CucE) is a highly oxidized steroid consisting of a tetracyclic triterpene. It is a member of a Cucurbitacin family of biomolecules that are predominantly found in Cucurbitaceae plants. CucE has already been identified as a potent anti-inflammatory compound. Here, its effects on CD4(+) T helper (Th) cells and macrophages, as the major encephalitogenic cells in the autoimmunity of the central nervous system, were investigated. Production of major pathogenic Th cell cytokines: interferon-gamma and interleukin-17 were inhibited under the influence of CucE. The effects of CucE on CD4+ T cells were mediated through the modulation of aryl hydrocarbon receptor, STAT3, Na kappa B, p38 MAPK, and miR-146 signaling. Further, production of nitric oxide and reactive oxygen species, as well as phagocytic ability, were inhibited in macrophages treated with CucE. These results imply that CucE possesses powerful antiencephalitogenic activity.",
publisher = "Amer Chemical Soc, Washington",
journal = "Journal of Agricultural and Food Chemistry",
title = "Cucurbitacin E Potently Modulates the Activity of Encephalitogenic Cells",
pages = "4907-4900",
number = "24",
volume = "64",
doi = "10.1021/acs.jafc.6b00951"
}

Jevtić, B., Đedović, N., Stanisavljević, S., Despotović, J., Mijković, D.,& Timotijević, G.. (2016). Cucurbitacin E Potently Modulates the Activity of Encephalitogenic Cells. in Journal of Agricultural and Food Chemistry
Amer Chemical Soc, Washington., 64(24), 4900-4907.
https://doi.org/10.1021/acs.jafc.6b00951

Jevtić B, Đedović N, Stanisavljević S, Despotović J, Mijković D, Timotijević G. Cucurbitacin E Potently Modulates the Activity of Encephalitogenic Cells. in Journal of Agricultural and Food Chemistry. 2016;64(24):4900-4907.
doi:10.1021/acs.jafc.6b00951 .

Jevtić, Bojan, Đedović, Neda, Stanisavljević, Suzana, Despotović, Jovana, Mijković, Djordje, Timotijević, Gordana, "Cucurbitacin E Potently Modulates the Activity of Encephalitogenic Cells" in Journal of Agricultural and Food Chemistry, 64, no. 24 (2016):4900-4907,
https://doi.org/10.1021/acs.jafc.6b00951 . .

TY  - JOUR
AU  - Jevtić, Bojan
AU  - Timotijević, Gordana
AU  - Stanisavljević, Suzana
AU  - Momcilović, Miljana
AU  - Mostarica-Stojković, Marija
AU  - Miljković, Djordje
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/821
AB  - MicroRNAs (miR) are small non-coding RNAs involved in the immune response regulation. miR-155 has been attributed a major pro-inflammatory role in the pathogenesis of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Here, a role of miR-155 in re-activation of encephalitogenic CD4(+) T cells was investigated. Dark Agouti rats were immunized with myelin basic protein (MBP) emulsified in complete Freund's adjuvant. CD4(+) T cells were purified from draining lymph node cells (DLNC) obtained in the inductive phase and from spinal cord immune cells (SCIC) isolated at the peak of EAE. CD4(+) T cells obtained from SCIC (i.e., in vivo re-activated cells) had markedly higher expression of miR-155 in comparison to those purified from DLNC (not re-activated). Likewise, in vitro re-activation of DLNC with MBP led to increase in miR-155 expression. Further, DLNC and DLNC CD4(+) T cells were transfected with an inhibitor of miR-155 during in vitro re-activation. As a result, expression of important CD4(+) T cell effector cytokines IFN-gamma and IL-17, but not of regulatory cytokines IL-10 and TGF-beta, was reduced. These results imply that miR-155 supports re-activation of encephalitogenic CD4+ T cells. Our results contribute to a view that miR-155 might be a valuable target in multiple sclerosis therapy.
PB  - Elsevier France-Editions Scientifiques Medicales Elsevier, Paris
T2  - Biomedicine & Pharmacotherapy
T1  - Micro RNA-155 participates in re-activation of encephalitogenic T cells
EP  - 210
SP  - 206
VL  - 74
DO  - 10.1016/j.biopha.2015.08.011
ER  - 

@article{
author = "Jevtić, Bojan and Timotijević, Gordana and Stanisavljević, Suzana and Momcilović, Miljana and Mostarica-Stojković, Marija and Miljković, Djordje",
year = "2015",
abstract = "MicroRNAs (miR) are small non-coding RNAs involved in the immune response regulation. miR-155 has been attributed a major pro-inflammatory role in the pathogenesis of multiple sclerosis and its animal model experimental autoimmune encephalomyelitis (EAE). Here, a role of miR-155 in re-activation of encephalitogenic CD4(+) T cells was investigated. Dark Agouti rats were immunized with myelin basic protein (MBP) emulsified in complete Freund's adjuvant. CD4(+) T cells were purified from draining lymph node cells (DLNC) obtained in the inductive phase and from spinal cord immune cells (SCIC) isolated at the peak of EAE. CD4(+) T cells obtained from SCIC (i.e., in vivo re-activated cells) had markedly higher expression of miR-155 in comparison to those purified from DLNC (not re-activated). Likewise, in vitro re-activation of DLNC with MBP led to increase in miR-155 expression. Further, DLNC and DLNC CD4(+) T cells were transfected with an inhibitor of miR-155 during in vitro re-activation. As a result, expression of important CD4(+) T cell effector cytokines IFN-gamma and IL-17, but not of regulatory cytokines IL-10 and TGF-beta, was reduced. These results imply that miR-155 supports re-activation of encephalitogenic CD4+ T cells. Our results contribute to a view that miR-155 might be a valuable target in multiple sclerosis therapy.",
publisher = "Elsevier France-Editions Scientifiques Medicales Elsevier, Paris",
journal = "Biomedicine & Pharmacotherapy",
title = "Micro RNA-155 participates in re-activation of encephalitogenic T cells",
pages = "210-206",
volume = "74",
doi = "10.1016/j.biopha.2015.08.011"
}

Jevtić, B., Timotijević, G., Stanisavljević, S., Momcilović, M., Mostarica-Stojković, M.,& Miljković, D.. (2015). Micro RNA-155 participates in re-activation of encephalitogenic T cells. in Biomedicine & Pharmacotherapy
Elsevier France-Editions Scientifiques Medicales Elsevier, Paris., 74, 206-210.
https://doi.org/10.1016/j.biopha.2015.08.011

Jevtić B, Timotijević G, Stanisavljević S, Momcilović M, Mostarica-Stojković M, Miljković D. Micro RNA-155 participates in re-activation of encephalitogenic T cells. in Biomedicine & Pharmacotherapy. 2015;74:206-210.
doi:10.1016/j.biopha.2015.08.011 .

Jevtić, Bojan, Timotijević, Gordana, Stanisavljević, Suzana, Momcilović, Miljana, Mostarica-Stojković, Marija, Miljković, Djordje, "Micro RNA-155 participates in re-activation of encephalitogenic T cells" in Biomedicine & Pharmacotherapy, 74 (2015):206-210,
https://doi.org/10.1016/j.biopha.2015.08.011 . .

TY  - JOUR
AU  - Petković, F.
AU  - Zivanović, J.
AU  - Blazevski, J.
AU  - Timotijević, Gordana
AU  - Momcilović, M.
AU  - Stanojević, Z.
AU  - Stamenković, V.
AU  - Milosević, V.
AU  - Mostarica-Stojković, Marija
AU  - Miljković, D.
PY  - 2015
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/844
AB  - Experimental autoimmune encephalomyelitis (EAE) is a model of multiple sclerosis (MS), inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS). Clinically manifested EAE can be induced in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats by immunization with spinal cord homogenate (SCH) and complete Freund's adjuvant (CFA). Matrix metalloproteinases (MMP) play important roles in various steps of MS and EAE pathogenesis. Expression of gelatinases MMP2 and MMP9, their activator MMP14 and their inhibitor tissue inhibitor of MMP (TIMP) 1 in the CNS of AO and DA rats immunized with SCH + CFA was determined. Expression of mRNA for MMP2, MMP9 and MMP14 was higher and expression of TIMP1 mRNA was lower in AO rats. However, gelatinase activity in spinal cords was higher in samples obtained from DA rats. Further, while there was no strain difference in MMP2 and MMP9 mRNA expression in lymph nodes of the immunized rats, gelatinase activity was higher in DA rats. This activity was reduced by antiinflammatory cytokines interleukin (IL)-10 and IL-4. Interestingly, gelatinase activity was detected in the nuclei of cells within the CNS, but not of those in lymph nodes. Our results imply that posttranscriptional regulation of MMP2 and MMP9 expression and/or function determines low gelatinase activity within the CNS and in immune cells of EAE-resistant AO rats.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Neuroscience
T1  - Activity, but not MRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis
EP  - 12
SP  - 1
VL  - 292
DO  - 10.1016/j.neuroscience.2015.02.015
ER  - 

@article{
author = "Petković, F. and Zivanović, J. and Blazevski, J. and Timotijević, Gordana and Momcilović, M. and Stanojević, Z. and Stamenković, V. and Milosević, V. and Mostarica-Stojković, Marija and Miljković, D.",
year = "2015",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is a model of multiple sclerosis (MS), inflammatory, demyelinating and neurodegenerative disease of the central nervous system (CNS). Clinically manifested EAE can be induced in Dark Agouti (DA) rats, but not in Albino Oxford (AO) rats by immunization with spinal cord homogenate (SCH) and complete Freund's adjuvant (CFA). Matrix metalloproteinases (MMP) play important roles in various steps of MS and EAE pathogenesis. Expression of gelatinases MMP2 and MMP9, their activator MMP14 and their inhibitor tissue inhibitor of MMP (TIMP) 1 in the CNS of AO and DA rats immunized with SCH + CFA was determined. Expression of mRNA for MMP2, MMP9 and MMP14 was higher and expression of TIMP1 mRNA was lower in AO rats. However, gelatinase activity in spinal cords was higher in samples obtained from DA rats. Further, while there was no strain difference in MMP2 and MMP9 mRNA expression in lymph nodes of the immunized rats, gelatinase activity was higher in DA rats. This activity was reduced by antiinflammatory cytokines interleukin (IL)-10 and IL-4. Interestingly, gelatinase activity was detected in the nuclei of cells within the CNS, but not of those in lymph nodes. Our results imply that posttranscriptional regulation of MMP2 and MMP9 expression and/or function determines low gelatinase activity within the CNS and in immune cells of EAE-resistant AO rats.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Neuroscience",
title = "Activity, but not MRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis",
pages = "12-1",
volume = "292",
doi = "10.1016/j.neuroscience.2015.02.015"
}

Petković, F., Zivanović, J., Blazevski, J., Timotijević, G., Momcilović, M., Stanojević, Z., Stamenković, V., Milosević, V., Mostarica-Stojković, M.,& Miljković, D.. (2015). Activity, but not MRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis. in Neuroscience
Pergamon-Elsevier Science Ltd, Oxford., 292, 1-12.
https://doi.org/10.1016/j.neuroscience.2015.02.015

Petković F, Zivanović J, Blazevski J, Timotijević G, Momcilović M, Stanojević Z, Stamenković V, Milosević V, Mostarica-Stojković M, Miljković D. Activity, but not MRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis. in Neuroscience. 2015;292:1-12.
doi:10.1016/j.neuroscience.2015.02.015 .

Petković, F., Zivanović, J., Blazevski, J., Timotijević, Gordana, Momcilović, M., Stanojević, Z., Stamenković, V., Milosević, V., Mostarica-Stojković, Marija, Miljković, D., "Activity, but not MRNA expression of gelatinases correlates with susceptibility to experimental autoimmune encephalomyelitis" in Neuroscience, 292 (2015):1-12,
https://doi.org/10.1016/j.neuroscience.2015.02.015 . .

TY  - THES
AU  - Nikolić, Ivana G.
PY  - 2014
UR  - https://nardus.mpn.gov.rs/handle/123456789/4621
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=2431
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:10440/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=70036&RID=1024815794
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/36
AB  - Dijabetes tipa 1 (DT1) je autoimunsko inflamatorno oboljenje koje se razvija kao posledica uništavanja  ćelija pankreasa posredstvom autoagresivnih ćelija i njihovih pro-inflamatornih medijatora. Glavno obeležje DT1 je insulitis – infiltracija pankreasa populacijama imunskih ćelija. Makrofagi se smatraju prvim ćelijama koje infiltriraju pankreasna ostrvca i imaju važnu ulogu u aktivaciji autoreaktivnih T ćelija. Smatra se da klasiĉno aktivisani M1 makrofagi doprinose razvoju i progresiji bolesti, dok alternativno aktivisani M2 makrofagi uĉestvuju u njenom spreĉavanju. B limfociti imaju ulogu u produkciji autoantitela, dok su T (CD4+ i CD8+) ćelije jedne od glavnih efektorskih ćelija koje su ukljuĉene u ubijanje  ćelija. Citokini koje sekretuju razliĉite imunske ćelije, ukljuĉujući makrofage i T ćelije, mogu da regulišu u kom smeru će se razviti imunski odgovor: ka Th1 (engl. T helper) dijabetogenom odgovoru ili Th2 protektivnom odgovoru. Aktivisani makrofagi, pomoćniĉki i citotoksiĉni T limfociti, kao i sekretovani pro-inflamatorni medijatori, sinergistiĉki uĉestvuju u razaranju  ćelija i razliĉitim mehanizmima pokreću apoptozu ovih ćelija, što rezultuje nastankom autoimunskog DT1. Kako terapija DT1 uglavnom podrazumeva primenu egzogenog insulina, sve više se istražuju novi terapijski pristupi koji bi spreĉili ili usporili pokrenuti autoimunski odgovor. Ugljen monoksid (CO) je potencijalni kandidat za tretman autoimunskih bolesti, kao što je DT1, zbog svojih anti-inflamatornih i antiapoptotskih karakteristika. CO nastaje u organizmu delovanjem enzima hem oksigenaze (HO) koja razgraĊuje hem do CO, biliverdina i gvožĊa. Uprkos izuzetnoj toksiĉnosti u visokim koncentracijama, primenjen u niskim koncentracijama egzogeni CO ima terapijski potencijal kao anti-inflamatorni agens koji moduliše brojna imunoinflamatorna stanja. Sintetisana metalo-organska jedinjenja koja oslobaĊaju CO (CORM engl. Carbon Monoxide Releasnig Molecule) predstavljaju grupu jedinjenja sposobnih da otpuštaju CO na kontrolisani naĉin u ćelijskim sistemima. Jedno od brojnih CORM je i CORM-A1 koji se izdvaja od ostalih jedinjenja jer je rastvorljiv u vodi, ne sadrži prelazne metale u svojoj strukturi i vreme poluživota ovog jedinjenja u fiziološkim uslovima je 21,4 minut...
AB  - Type 1 diabetes (T1D), an autoimmune inflammatory disorder, develops as a consequence of pancreatic beta cell destruction mediated by various pro-inflammatory mediators. The major hallmark of T1D is infiltration of different populations of immune cells into pancreas called insulitis. Macrophages are the first cell types to infiltrate the pancreatic islets and play essential role in the development and activation of autoreactive T cells. Classically activated M1 macrophages are involved in disease development and progression, while alternatively activated M2 macrophages participate in disease suppression. B lymphocytes produce autoantibodies against pancreatic  cell antigens, and T cells are known to play a crucial role as final effectors that kill  cells. Cytokines secreted by various immune cells, including macrophages and T cells, may regulate the direction of the immune response toward helper T (Th) 1 cells, related to diabetes development, or Th2 response, which has protective role in T1D. Therefore, the activated macrophages, Th and cytotoxic T cells, as well as secreted proinflammatory mediators, act synergistically in destruction of  cells through different mechanisms, resulting in development of autoimmune T1D. Since current T1D therapy mainly involves insulin replacement, constant efforts are being directed toward establishing novel therapeutic approaches that could inhibit or suppress autoimmune response. Carbon monoxide (CO) could be a potential therapeutic molecule for the treatment of autoimmune diseases, such as T1D, due to its anti-inflammatory and antiapoptotic abilities. CO, together with biliverdin and iron, arises endogenously from degradation of heme molecules by heme oxygenase (HO) enzyme. Despite extreme toxicity when given at high concentrations, exogenous CO delivered at low concentrations is showing therapeutic potential as an anti-inflammatory agent and, as such, can modulate numerous immunoinflammatory states. The carbon monoxidereleasing molecules (CORMs) represent a group of compounds capable of liberating controlled quantities of CO in the cellular systems...
PB  - Univerzitet u Beogradu, Biološki fakultet
T1  - Uloga donora ugljen-monoksida CORM-A1 u modulaciji eksperimentalno indukovanog dijabetesa tipa 1 kod C57BL/6 miševa
T1  - The role of carbon monoxide-releasing molecule CORM-A1 in modulation of experimentally induced type 1 diabetes in C57BL/6 mice.
UR  - https://hdl.handle.net/21.15107/rcub_nardus_4621
ER  - 

@phdthesis{
author = "Nikolić, Ivana G.",
year = "2014",
abstract = "Dijabetes tipa 1 (DT1) je autoimunsko inflamatorno oboljenje koje se razvija kao posledica uništavanja  ćelija pankreasa posredstvom autoagresivnih ćelija i njihovih pro-inflamatornih medijatora. Glavno obeležje DT1 je insulitis – infiltracija pankreasa populacijama imunskih ćelija. Makrofagi se smatraju prvim ćelijama koje infiltriraju pankreasna ostrvca i imaju važnu ulogu u aktivaciji autoreaktivnih T ćelija. Smatra se da klasiĉno aktivisani M1 makrofagi doprinose razvoju i progresiji bolesti, dok alternativno aktivisani M2 makrofagi uĉestvuju u njenom spreĉavanju. B limfociti imaju ulogu u produkciji autoantitela, dok su T (CD4+ i CD8+) ćelije jedne od glavnih efektorskih ćelija koje su ukljuĉene u ubijanje  ćelija. Citokini koje sekretuju razliĉite imunske ćelije, ukljuĉujući makrofage i T ćelije, mogu da regulišu u kom smeru će se razviti imunski odgovor: ka Th1 (engl. T helper) dijabetogenom odgovoru ili Th2 protektivnom odgovoru. Aktivisani makrofagi, pomoćniĉki i citotoksiĉni T limfociti, kao i sekretovani pro-inflamatorni medijatori, sinergistiĉki uĉestvuju u razaranju  ćelija i razliĉitim mehanizmima pokreću apoptozu ovih ćelija, što rezultuje nastankom autoimunskog DT1. Kako terapija DT1 uglavnom podrazumeva primenu egzogenog insulina, sve više se istražuju novi terapijski pristupi koji bi spreĉili ili usporili pokrenuti autoimunski odgovor. Ugljen monoksid (CO) je potencijalni kandidat za tretman autoimunskih bolesti, kao što je DT1, zbog svojih anti-inflamatornih i antiapoptotskih karakteristika. CO nastaje u organizmu delovanjem enzima hem oksigenaze (HO) koja razgraĊuje hem do CO, biliverdina i gvožĊa. Uprkos izuzetnoj toksiĉnosti u visokim koncentracijama, primenjen u niskim koncentracijama egzogeni CO ima terapijski potencijal kao anti-inflamatorni agens koji moduliše brojna imunoinflamatorna stanja. Sintetisana metalo-organska jedinjenja koja oslobaĊaju CO (CORM engl. Carbon Monoxide Releasnig Molecule) predstavljaju grupu jedinjenja sposobnih da otpuštaju CO na kontrolisani naĉin u ćelijskim sistemima. Jedno od brojnih CORM je i CORM-A1 koji se izdvaja od ostalih jedinjenja jer je rastvorljiv u vodi, ne sadrži prelazne metale u svojoj strukturi i vreme poluživota ovog jedinjenja u fiziološkim uslovima je 21,4 minut..., Type 1 diabetes (T1D), an autoimmune inflammatory disorder, develops as a consequence of pancreatic beta cell destruction mediated by various pro-inflammatory mediators. The major hallmark of T1D is infiltration of different populations of immune cells into pancreas called insulitis. Macrophages are the first cell types to infiltrate the pancreatic islets and play essential role in the development and activation of autoreactive T cells. Classically activated M1 macrophages are involved in disease development and progression, while alternatively activated M2 macrophages participate in disease suppression. B lymphocytes produce autoantibodies against pancreatic  cell antigens, and T cells are known to play a crucial role as final effectors that kill  cells. Cytokines secreted by various immune cells, including macrophages and T cells, may regulate the direction of the immune response toward helper T (Th) 1 cells, related to diabetes development, or Th2 response, which has protective role in T1D. Therefore, the activated macrophages, Th and cytotoxic T cells, as well as secreted proinflammatory mediators, act synergistically in destruction of  cells through different mechanisms, resulting in development of autoimmune T1D. Since current T1D therapy mainly involves insulin replacement, constant efforts are being directed toward establishing novel therapeutic approaches that could inhibit or suppress autoimmune response. Carbon monoxide (CO) could be a potential therapeutic molecule for the treatment of autoimmune diseases, such as T1D, due to its anti-inflammatory and antiapoptotic abilities. CO, together with biliverdin and iron, arises endogenously from degradation of heme molecules by heme oxygenase (HO) enzyme. Despite extreme toxicity when given at high concentrations, exogenous CO delivered at low concentrations is showing therapeutic potential as an anti-inflammatory agent and, as such, can modulate numerous immunoinflammatory states. The carbon monoxidereleasing molecules (CORMs) represent a group of compounds capable of liberating controlled quantities of CO in the cellular systems...",
publisher = "Univerzitet u Beogradu, Biološki fakultet",
title = "Uloga donora ugljen-monoksida CORM-A1 u modulaciji eksperimentalno indukovanog dijabetesa tipa 1 kod C57BL/6 miševa, The role of carbon monoxide-releasing molecule CORM-A1 in modulation of experimentally induced type 1 diabetes in C57BL/6 mice.",
url = "https://hdl.handle.net/21.15107/rcub_nardus_4621"
}

Nikolić, I. G.. (2014). Uloga donora ugljen-monoksida CORM-A1 u modulaciji eksperimentalno indukovanog dijabetesa tipa 1 kod C57BL/6 miševa. 
Univerzitet u Beogradu, Biološki fakultet..
https://hdl.handle.net/21.15107/rcub_nardus_4621

Nikolić IG. Uloga donora ugljen-monoksida CORM-A1 u modulaciji eksperimentalno indukovanog dijabetesa tipa 1 kod C57BL/6 miševa. 2014;.
https://hdl.handle.net/21.15107/rcub_nardus_4621 .

Nikolić, Ivana G., "Uloga donora ugljen-monoksida CORM-A1 u modulaciji eksperimentalno indukovanog dijabetesa tipa 1 kod C57BL/6 miševa" (2014),
https://hdl.handle.net/21.15107/rcub_nardus_4621 .

TY  - JOUR
AU  - Nikodinović-Runić, Jasmina
AU  - Mojić, Marija
AU  - Kang, Yijin
AU  - Maksimović-Ivanić, Danijela
AU  - Mijatović, Sanja
AU  - Vasiljević, Branka
AU  - Stamenković, Vojislav R.
AU  - Šenerović, Lidija
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/719
AB  - Bacterial pigment undecylprodigiosin (UP) was produced using Streptomyces sp. JS520 and conjugated to monodisperse gold nanoparticles (UP-Au). Both UP and UP-Au showed cytocidal activity towards melanoma (A375), lung carcinoma (A549), breast cancer (MCF-7) and colon cancer (HCT-116) cells, inducing apoptosis with IC50 values ranging from 0.4 to 4 mu g ml(-1). Unconjugated UP had a tendency to lose its activity over time and to change biophysical characteristics over pH. The loss of the pigment potency was overcome by conjugation with gold nanoparticles. UP-Au exhibited high stability over pH 3.8 to 7.4 and its activity remained unaffected in time. Nano-packing changed the mechanism of UP toxicity by converting the intracellular signals from a mitochondrial dependent to a mitochondrial independent apoptotic process. The availability of nonpyrogenic UP in high amounts, together with specific anticancer activity and improved stability in the complex with gold nanoparticles, presents a novel platform for further development of UP-Au complexes as an anticancer drug suitable for clinical applications.
PB  - Royal Soc Chemistry, Cambridge
T2  - Journal of Materials Chemistry B
T1  - Undecylprodigiosin conjugated monodisperse gold nanoparticles efficiently cause apoptosis in colon cancer cells in vitro
EP  - 3281
IS  - 21
SP  - 3271
VL  - 2
DO  - 10.1039/c4tb00300d
ER  - 

@article{
author = "Nikodinović-Runić, Jasmina and Mojić, Marija and Kang, Yijin and Maksimović-Ivanić, Danijela and Mijatović, Sanja and Vasiljević, Branka and Stamenković, Vojislav R. and Šenerović, Lidija",
year = "2014",
abstract = "Bacterial pigment undecylprodigiosin (UP) was produced using Streptomyces sp. JS520 and conjugated to monodisperse gold nanoparticles (UP-Au). Both UP and UP-Au showed cytocidal activity towards melanoma (A375), lung carcinoma (A549), breast cancer (MCF-7) and colon cancer (HCT-116) cells, inducing apoptosis with IC50 values ranging from 0.4 to 4 mu g ml(-1). Unconjugated UP had a tendency to lose its activity over time and to change biophysical characteristics over pH. The loss of the pigment potency was overcome by conjugation with gold nanoparticles. UP-Au exhibited high stability over pH 3.8 to 7.4 and its activity remained unaffected in time. Nano-packing changed the mechanism of UP toxicity by converting the intracellular signals from a mitochondrial dependent to a mitochondrial independent apoptotic process. The availability of nonpyrogenic UP in high amounts, together with specific anticancer activity and improved stability in the complex with gold nanoparticles, presents a novel platform for further development of UP-Au complexes as an anticancer drug suitable for clinical applications.",
publisher = "Royal Soc Chemistry, Cambridge",
journal = "Journal of Materials Chemistry B",
title = "Undecylprodigiosin conjugated monodisperse gold nanoparticles efficiently cause apoptosis in colon cancer cells in vitro",
pages = "3281-3271",
number = "21",
volume = "2",
doi = "10.1039/c4tb00300d"
}

Nikodinović-Runić, J., Mojić, M., Kang, Y., Maksimović-Ivanić, D., Mijatović, S., Vasiljević, B., Stamenković, V. R.,& Šenerović, L.. (2014). Undecylprodigiosin conjugated monodisperse gold nanoparticles efficiently cause apoptosis in colon cancer cells in vitro. in Journal of Materials Chemistry B
Royal Soc Chemistry, Cambridge., 2(21), 3271-3281.
https://doi.org/10.1039/c4tb00300d

Nikodinović-Runić J, Mojić M, Kang Y, Maksimović-Ivanić D, Mijatović S, Vasiljević B, Stamenković VR, Šenerović L. Undecylprodigiosin conjugated monodisperse gold nanoparticles efficiently cause apoptosis in colon cancer cells in vitro. in Journal of Materials Chemistry B. 2014;2(21):3271-3281.
doi:10.1039/c4tb00300d .

Nikodinović-Runić, Jasmina, Mojić, Marija, Kang, Yijin, Maksimović-Ivanić, Danijela, Mijatović, Sanja, Vasiljević, Branka, Stamenković, Vojislav R., Šenerović, Lidija, "Undecylprodigiosin conjugated monodisperse gold nanoparticles efficiently cause apoptosis in colon cancer cells in vitro" in Journal of Materials Chemistry B, 2, no. 21 (2014):3271-3281,
https://doi.org/10.1039/c4tb00300d . .

TY  - JOUR
AU  - Vujicić, Milica
AU  - Šenerović, Lidija
AU  - Nikolić, Ivana
AU  - Saksida, Tamara
AU  - Stošić-Grujičić, Stanislava
AU  - Stojanović, Ivana
PY  - 2014
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/717
AB  - Macrophage migration inhibitory factor (MIF) is a molecule with plethora of functions such as regulation of immune response, hormone-like, enzymatic and chaperone-like activity. Further, MIF is a major participant in glucose homeostasis since it is an autocrine stimulator of insulin secretion. MIF absence in male knockout mice (MW-MO) results in development of glucose intolerance, while sensitivity to insulin is fully preserved. Since our results confirm that beta cells from MIF-KO mice express, produce and secrete insulin similarly to beta cells of their wild type (WT) counterparts C57BL/6 mice, we hypothesize that MIF-KO-derived insulin is less active. Indeed, insulin from MIF-KO islets is unable to significantly induce glucose uptake into hepatocytes and to efficiently promote insulin-triggered Akt phosphorylation determined by immunoblot. However, MIF's tautomerase function is not crucial for insulin biosynthesis since MIF inhibitors had no impact on WT insulin activity. Importantly, MIF recognition by anti-MIF anti-body (ELISA) after in vitro co-incubation with purified insulin was significantly lower suggesting that insulin covers MIF immunodominant epitope. In addition, MIF binds insulin within beta cell as confirmed by co-immunoprecipitation. WT and MIF-KO-derived insulin exhibited different cleavage patterns suggesting different protein conformations. Finally, pre-incubation of recombinant MIF with insulin promotes formation of insulin hexamers. These results imply that MIF probably enables proper insulin folding what results in insulin full activity. This newly discovered feature of the cytokine MIF could be potentially important for commercially produced insulin, for increasing its stability and/or bioavailability.
PB  - Academic Press Ltd- Elsevier Science Ltd, London
T2  - Cytokine
T1  - The critical role of macrophage migration inhibitory factor in insulin activity
EP  - 46
IS  - 1
SP  - 39
VL  - 69
DO  - 10.1016/j.cyto.2014.05.013
ER  - 

@article{
author = "Vujicić, Milica and Šenerović, Lidija and Nikolić, Ivana and Saksida, Tamara and Stošić-Grujičić, Stanislava and Stojanović, Ivana",
year = "2014",
abstract = "Macrophage migration inhibitory factor (MIF) is a molecule with plethora of functions such as regulation of immune response, hormone-like, enzymatic and chaperone-like activity. Further, MIF is a major participant in glucose homeostasis since it is an autocrine stimulator of insulin secretion. MIF absence in male knockout mice (MW-MO) results in development of glucose intolerance, while sensitivity to insulin is fully preserved. Since our results confirm that beta cells from MIF-KO mice express, produce and secrete insulin similarly to beta cells of their wild type (WT) counterparts C57BL/6 mice, we hypothesize that MIF-KO-derived insulin is less active. Indeed, insulin from MIF-KO islets is unable to significantly induce glucose uptake into hepatocytes and to efficiently promote insulin-triggered Akt phosphorylation determined by immunoblot. However, MIF's tautomerase function is not crucial for insulin biosynthesis since MIF inhibitors had no impact on WT insulin activity. Importantly, MIF recognition by anti-MIF anti-body (ELISA) after in vitro co-incubation with purified insulin was significantly lower suggesting that insulin covers MIF immunodominant epitope. In addition, MIF binds insulin within beta cell as confirmed by co-immunoprecipitation. WT and MIF-KO-derived insulin exhibited different cleavage patterns suggesting different protein conformations. Finally, pre-incubation of recombinant MIF with insulin promotes formation of insulin hexamers. These results imply that MIF probably enables proper insulin folding what results in insulin full activity. This newly discovered feature of the cytokine MIF could be potentially important for commercially produced insulin, for increasing its stability and/or bioavailability.",
publisher = "Academic Press Ltd- Elsevier Science Ltd, London",
journal = "Cytokine",
title = "The critical role of macrophage migration inhibitory factor in insulin activity",
pages = "46-39",
number = "1",
volume = "69",
doi = "10.1016/j.cyto.2014.05.013"
}

Vujicić, M., Šenerović, L., Nikolić, I., Saksida, T., Stošić-Grujičić, S.,& Stojanović, I.. (2014). The critical role of macrophage migration inhibitory factor in insulin activity. in Cytokine
Academic Press Ltd- Elsevier Science Ltd, London., 69(1), 39-46.
https://doi.org/10.1016/j.cyto.2014.05.013

Vujicić M, Šenerović L, Nikolić I, Saksida T, Stošić-Grujičić S, Stojanović I. The critical role of macrophage migration inhibitory factor in insulin activity. in Cytokine. 2014;69(1):39-46.
doi:10.1016/j.cyto.2014.05.013 .

Vujicić, Milica, Šenerović, Lidija, Nikolić, Ivana, Saksida, Tamara, Stošić-Grujičić, Stanislava, Stojanović, Ivana, "The critical role of macrophage migration inhibitory factor in insulin activity" in Cytokine, 69, no. 1 (2014):39-46,
https://doi.org/10.1016/j.cyto.2014.05.013 . .

TY  - JOUR
AU  - Timotijević, Gordana
AU  - Petković, Filip
AU  - Blazevski, Jana
AU  - Momcilović, Miljana
AU  - Mostarica-Stojković, Marija
AU  - Miljković, Djordje
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/654
AB  - CXCL12 plays a protective role in CNS autoimmunity. Expression of CXCL12-gamma, which has distinct structural and functional properties than the other isoforms of CXCL12, was determined in spinal cords of rats immunized to develop experimental autoimmune encephalomyelitis (EAE). CNS expression of CXCL12-gamma was markedly lower in EAE-prone Dark Agouti rats than in EAE-resistant Albino Oxford rats, both in spinal cord homogenates and micro-blood vessels isolated from spinal cords. Inhibition of nitric oxide (NO) synthesis in DA rats upregulated, while donation of NO in AO rats downregulated CNS expression of CXCL12-gamma. NO inhibited CXCL12-gamma expression in astrocytes in vitro. A splice variant of CXCL12-gamma which migrates into nucleolus was not detected in spinal cord or astrocytes. Thus, CXCL12-gamma is expressed in the CNS after EAE induction, but its expression is markedly suppressed in spinal cord affected with full blown inflammation. NO is an important regulator of CXCL12-gamma expression in neuroinflammation.
PB  - Elsevier Science Bv, Amsterdam
T2  - Brain Research
T1  - CXCL12-gamma expression is inhibited in neuroinflammation
EP  - 126
SP  - 120
VL  - 1519
DO  - 10.1016/j.brainres.2013.04.056
ER  - 

@article{
author = "Timotijević, Gordana and Petković, Filip and Blazevski, Jana and Momcilović, Miljana and Mostarica-Stojković, Marija and Miljković, Djordje",
year = "2013",
abstract = "CXCL12 plays a protective role in CNS autoimmunity. Expression of CXCL12-gamma, which has distinct structural and functional properties than the other isoforms of CXCL12, was determined in spinal cords of rats immunized to develop experimental autoimmune encephalomyelitis (EAE). CNS expression of CXCL12-gamma was markedly lower in EAE-prone Dark Agouti rats than in EAE-resistant Albino Oxford rats, both in spinal cord homogenates and micro-blood vessels isolated from spinal cords. Inhibition of nitric oxide (NO) synthesis in DA rats upregulated, while donation of NO in AO rats downregulated CNS expression of CXCL12-gamma. NO inhibited CXCL12-gamma expression in astrocytes in vitro. A splice variant of CXCL12-gamma which migrates into nucleolus was not detected in spinal cord or astrocytes. Thus, CXCL12-gamma is expressed in the CNS after EAE induction, but its expression is markedly suppressed in spinal cord affected with full blown inflammation. NO is an important regulator of CXCL12-gamma expression in neuroinflammation.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Brain Research",
title = "CXCL12-gamma expression is inhibited in neuroinflammation",
pages = "126-120",
volume = "1519",
doi = "10.1016/j.brainres.2013.04.056"
}

Timotijević, G., Petković, F., Blazevski, J., Momcilović, M., Mostarica-Stojković, M.,& Miljković, D.. (2013). CXCL12-gamma expression is inhibited in neuroinflammation. in Brain Research
Elsevier Science Bv, Amsterdam., 1519, 120-126.
https://doi.org/10.1016/j.brainres.2013.04.056

Timotijević G, Petković F, Blazevski J, Momcilović M, Mostarica-Stojković M, Miljković D. CXCL12-gamma expression is inhibited in neuroinflammation. in Brain Research. 2013;1519:120-126.
doi:10.1016/j.brainres.2013.04.056 .

Timotijević, Gordana, Petković, Filip, Blazevski, Jana, Momcilović, Miljana, Mostarica-Stojković, Marija, Miljković, Djordje, "CXCL12-gamma expression is inhibited in neuroinflammation" in Brain Research, 1519 (2013):120-126,
https://doi.org/10.1016/j.brainres.2013.04.056 . .

TY  - JOUR
AU  - Petković, Filip
AU  - Blazevski, Jana
AU  - Momcilović, Miljana
AU  - Timotijević, Gordana
AU  - Zocca, Mai-Britt
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Mangano, Katia
AU  - Fagone, Paolo
AU  - Stošić-Grujičić, Stanislava
AU  - Nicoletti, Ferdinando
AU  - Miljković, Djordje
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/647
AB  - NO-hybridization of the HIV protease inhibitor Saquinavir generates a new chemical entity named Saq-NO, that retains the anti-viral activity and exerts lower toxicity. We show that Saq-NO inhibited the generation of various cytokines in ConA-stimulated unfractionated murine spleen cells and rat lymph nodes stimulated with ConA as well as in purified CD4(+) T cells in vitro and reduced the circulating levels of cytokines in mice challenged with anti-CD3 antibody. Furthermore, Saq-NO reduced IL-17 and IFN-gamma production in myelin basic protein (MBP)-specific cells isolated from rats immunized with MBP. These findings translated well into the in vivo setting as Saq-NO ameliorated the course of the disease in two preclinical models of multiple sclerosis. Our results demonstrate that Saq-NO exerts immunomodulatory effects that warrant studies on its application in autoimmune diseases.
PB  - Elsevier Science Bv, Amsterdam
T2  - Journal of Neuroimmunology
T1  - Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis
EP  - 65
IS  - 1-2
SP  - 55
VL  - 259
DO  - 10.1016/j.jneuroim.2013.03.010
ER  - 

@article{
author = "Petković, Filip and Blazevski, Jana and Momcilović, Miljana and Timotijević, Gordana and Zocca, Mai-Britt and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Mangano, Katia and Fagone, Paolo and Stošić-Grujičić, Stanislava and Nicoletti, Ferdinando and Miljković, Djordje",
year = "2013",
abstract = "NO-hybridization of the HIV protease inhibitor Saquinavir generates a new chemical entity named Saq-NO, that retains the anti-viral activity and exerts lower toxicity. We show that Saq-NO inhibited the generation of various cytokines in ConA-stimulated unfractionated murine spleen cells and rat lymph nodes stimulated with ConA as well as in purified CD4(+) T cells in vitro and reduced the circulating levels of cytokines in mice challenged with anti-CD3 antibody. Furthermore, Saq-NO reduced IL-17 and IFN-gamma production in myelin basic protein (MBP)-specific cells isolated from rats immunized with MBP. These findings translated well into the in vivo setting as Saq-NO ameliorated the course of the disease in two preclinical models of multiple sclerosis. Our results demonstrate that Saq-NO exerts immunomodulatory effects that warrant studies on its application in autoimmune diseases.",
publisher = "Elsevier Science Bv, Amsterdam",
journal = "Journal of Neuroimmunology",
title = "Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis",
pages = "65-55",
number = "1-2",
volume = "259",
doi = "10.1016/j.jneuroim.2013.03.010"
}

Petković, F., Blazevski, J., Momcilović, M., Timotijević, G., Zocca, M., Mijatović, S., Maksimović-Ivanić, D., Mangano, K., Fagone, P., Stošić-Grujičić, S., Nicoletti, F.,& Miljković, D.. (2013). Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology
Elsevier Science Bv, Amsterdam., 259(1-2), 55-65.
https://doi.org/10.1016/j.jneuroim.2013.03.010

Petković F, Blazevski J, Momcilović M, Timotijević G, Zocca M, Mijatović S, Maksimović-Ivanić D, Mangano K, Fagone P, Stošić-Grujičić S, Nicoletti F, Miljković D. Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology. 2013;259(1-2):55-65.
doi:10.1016/j.jneuroim.2013.03.010 .

Petković, Filip, Blazevski, Jana, Momcilović, Miljana, Timotijević, Gordana, Zocca, Mai-Britt, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Mangano, Katia, Fagone, Paolo, Stošić-Grujičić, Stanislava, Nicoletti, Ferdinando, Miljković, Djordje, "Saquinavir-NO inhibits S6 kinase activity, impairs secretion of the encephalytogenic cytokines interleukin-17 and interferon-gamma and ameliorates experimental autoimmune encephalomyelitis" in Journal of Neuroimmunology, 259, no. 1-2 (2013):55-65,
https://doi.org/10.1016/j.jneuroim.2013.03.010 . .

TY  - JOUR
AU  - Saksida, Tamara
AU  - Miljković, Djordje
AU  - Timotijević, Gordana
AU  - Stojanović, Ivana
AU  - Mijatović, Sanja
AU  - Fagone, Paolo
AU  - Mangano, Katia
AU  - Mammana, Santa
AU  - Farina, Claudio
AU  - Ascione, Ester
AU  - Maiello, Valentina
AU  - Nicoletti, Ferdinando
AU  - Stošić-Grujičić, Stanislava
PY  - 2013
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/627
AB  - Transferrin (Tf) has a major role in T cell activation and proliferation. Here, we investigated whether Tf exerts immunomodulatory effects on T cells and in development of T-cell driven experimental autoimmune encephalomyelitis (EAE). While treatment of concanavalin A-stimulated splenocytes with apotransferrin (ApoTf) did not affect release of IL-1 beta, TNF, INF-gamma, IL-17, IL-4, and IL-10, it markedly and dose-dependently down-regulated synthesis of IL-2 in these cells. ApoTf also inhibited IL-2 generation in purified CD3(+) T cells and the effect was accompanied with down-regulation of MAPK p44/42 and NF kappa B signaling. Despite impeded IL-2 release, proliferation of splenocytes was not inhibited by ApoTf. Importantly, ApoTf ameliorated EAE in mice and significantly reduced ex vivo IL-2 production in proteolipid protein-specific lymphocytes. Thus ApoTf may be a promising beneficial agent for multiple sclerosis.
PB  - Elsevier, Amsterdam
T2  - Journal of Neuroimmunology
T1  - Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis
EP  - 78
IS  - 1-2
SP  - 72
VL  - 262
DO  - 10.1016/j.jneuroim.2013.07.001
ER  - 

@article{
author = "Saksida, Tamara and Miljković, Djordje and Timotijević, Gordana and Stojanović, Ivana and Mijatović, Sanja and Fagone, Paolo and Mangano, Katia and Mammana, Santa and Farina, Claudio and Ascione, Ester and Maiello, Valentina and Nicoletti, Ferdinando and Stošić-Grujičić, Stanislava",
year = "2013",
abstract = "Transferrin (Tf) has a major role in T cell activation and proliferation. Here, we investigated whether Tf exerts immunomodulatory effects on T cells and in development of T-cell driven experimental autoimmune encephalomyelitis (EAE). While treatment of concanavalin A-stimulated splenocytes with apotransferrin (ApoTf) did not affect release of IL-1 beta, TNF, INF-gamma, IL-17, IL-4, and IL-10, it markedly and dose-dependently down-regulated synthesis of IL-2 in these cells. ApoTf also inhibited IL-2 generation in purified CD3(+) T cells and the effect was accompanied with down-regulation of MAPK p44/42 and NF kappa B signaling. Despite impeded IL-2 release, proliferation of splenocytes was not inhibited by ApoTf. Importantly, ApoTf ameliorated EAE in mice and significantly reduced ex vivo IL-2 production in proteolipid protein-specific lymphocytes. Thus ApoTf may be a promising beneficial agent for multiple sclerosis.",
publisher = "Elsevier, Amsterdam",
journal = "Journal of Neuroimmunology",
title = "Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis",
pages = "78-72",
number = "1-2",
volume = "262",
doi = "10.1016/j.jneuroim.2013.07.001"
}

Saksida, T., Miljković, D., Timotijević, G., Stojanović, I., Mijatović, S., Fagone, P., Mangano, K., Mammana, S., Farina, C., Ascione, E., Maiello, V., Nicoletti, F.,& Stošić-Grujičić, S.. (2013). Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology
Elsevier, Amsterdam., 262(1-2), 72-78.
https://doi.org/10.1016/j.jneuroim.2013.07.001

Saksida T, Miljković D, Timotijević G, Stojanović I, Mijatović S, Fagone P, Mangano K, Mammana S, Farina C, Ascione E, Maiello V, Nicoletti F, Stošić-Grujičić S. Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis. in Journal of Neuroimmunology. 2013;262(1-2):72-78.
doi:10.1016/j.jneuroim.2013.07.001 .

Saksida, Tamara, Miljković, Djordje, Timotijević, Gordana, Stojanović, Ivana, Mijatović, Sanja, Fagone, Paolo, Mangano, Katia, Mammana, Santa, Farina, Claudio, Ascione, Ester, Maiello, Valentina, Nicoletti, Ferdinando, Stošić-Grujičić, Stanislava, "Apotransferrin inhibits interleukin-2 expression and protects mice from experimental autoimmune encephalomyelitis" in Journal of Neuroimmunology, 262, no. 1-2 (2013):72-78,
https://doi.org/10.1016/j.jneuroim.2013.07.001 . .

TY  - JOUR
AU  - Saksida, Tamara
AU  - Stošić-Grujičić, Stanislava
AU  - Timotijević, Gordana
AU  - Sandler, Stellan
AU  - Stojanović, Ivana
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/552
AB  - As a result of chronic exposure to high levels of free fatty acids, glucose and inflammatory mediators beta-cell apoptosis occurs at the end stage of obesity-associated type 2 diabetes (T2D). One potentially deleterious molecule for beta-cell function associated with T2D and obesity in humans is macrophage migration inhibitory factor (MIF). Therefore, the aim of this study was to explore MIF expression in vivo during development of obesity and insulin resistance in high-fat diet (HFD)-fed C57BL/6 mice and whether MIF inhibition could affect beta-cell apoptosis and dysfunction induced by palmitic acid (PA) in vitro. Indeed, increase in systemic and locally produced MIF correlated well with the weight gain, triglyceride upregulation, glucose intolerance and insulin resistance, which developed in HFD-fed mice. In in vitro settings PA dose-dependently induced MIF secretion before apoptosis development in islets. Further, mif gene deletion, mRNA silencing or protein inhibition rescued beta-cells from PA-induced apoptosis as measured by MTT assay and histone-DNA enzyme linked immuno sorbent assay. Protection from induced apoptosis was mediated by altered activation of caspase pathway and correlated with changes in the level of Bcl-2 family members. Further, MIF inhibition conveyed a significant resistance to PA-induced downregulation of insulin and PDX-1 expression and ATP content. However, beta-cell function was not entirely preserved in the absence of MIF judging by low glucose oxidation and depolarized mitochondria! membrane. In conclusion, the observed considerable preservation of beta-cells from nutrient-induced apoptosis might implicate MIF as a potential therapeutic target in the later stage of obesity-associated T2D. Immunology and Cell Biology (2012) 90, 688-698; doi:10.1038/icb.2011.89; published online 8 November 2011
PB  - Wiley, Hoboken
T2  - Immunology and Cell Biology
T1  - Macrophage migration inhibitory factor deficiency protects pancreatic islets from palmitic acid-induced apoptosis
EP  - 698
IS  - 7
SP  - 688
VL  - 90
DO  - 10.1038/icb.2011.89
ER  - 

@article{
author = "Saksida, Tamara and Stošić-Grujičić, Stanislava and Timotijević, Gordana and Sandler, Stellan and Stojanović, Ivana",
year = "2012",
abstract = "As a result of chronic exposure to high levels of free fatty acids, glucose and inflammatory mediators beta-cell apoptosis occurs at the end stage of obesity-associated type 2 diabetes (T2D). One potentially deleterious molecule for beta-cell function associated with T2D and obesity in humans is macrophage migration inhibitory factor (MIF). Therefore, the aim of this study was to explore MIF expression in vivo during development of obesity and insulin resistance in high-fat diet (HFD)-fed C57BL/6 mice and whether MIF inhibition could affect beta-cell apoptosis and dysfunction induced by palmitic acid (PA) in vitro. Indeed, increase in systemic and locally produced MIF correlated well with the weight gain, triglyceride upregulation, glucose intolerance and insulin resistance, which developed in HFD-fed mice. In in vitro settings PA dose-dependently induced MIF secretion before apoptosis development in islets. Further, mif gene deletion, mRNA silencing or protein inhibition rescued beta-cells from PA-induced apoptosis as measured by MTT assay and histone-DNA enzyme linked immuno sorbent assay. Protection from induced apoptosis was mediated by altered activation of caspase pathway and correlated with changes in the level of Bcl-2 family members. Further, MIF inhibition conveyed a significant resistance to PA-induced downregulation of insulin and PDX-1 expression and ATP content. However, beta-cell function was not entirely preserved in the absence of MIF judging by low glucose oxidation and depolarized mitochondria! membrane. In conclusion, the observed considerable preservation of beta-cells from nutrient-induced apoptosis might implicate MIF as a potential therapeutic target in the later stage of obesity-associated T2D. Immunology and Cell Biology (2012) 90, 688-698; doi:10.1038/icb.2011.89; published online 8 November 2011",
publisher = "Wiley, Hoboken",
journal = "Immunology and Cell Biology",
title = "Macrophage migration inhibitory factor deficiency protects pancreatic islets from palmitic acid-induced apoptosis",
pages = "698-688",
number = "7",
volume = "90",
doi = "10.1038/icb.2011.89"
}

Saksida, T., Stošić-Grujičić, S., Timotijević, G., Sandler, S.,& Stojanović, I.. (2012). Macrophage migration inhibitory factor deficiency protects pancreatic islets from palmitic acid-induced apoptosis. in Immunology and Cell Biology
Wiley, Hoboken., 90(7), 688-698.
https://doi.org/10.1038/icb.2011.89

Saksida T, Stošić-Grujičić S, Timotijević G, Sandler S, Stojanović I. Macrophage migration inhibitory factor deficiency protects pancreatic islets from palmitic acid-induced apoptosis. in Immunology and Cell Biology. 2012;90(7):688-698.
doi:10.1038/icb.2011.89 .

Saksida, Tamara, Stošić-Grujičić, Stanislava, Timotijević, Gordana, Sandler, Stellan, Stojanović, Ivana, "Macrophage migration inhibitory factor deficiency protects pancreatic islets from palmitic acid-induced apoptosis" in Immunology and Cell Biology, 90, no. 7 (2012):688-698,
https://doi.org/10.1038/icb.2011.89 . .

TY  - JOUR
AU  - Mojić, Marija
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Miljković, Djordje
AU  - Stošić-Grujičić, Stanislava
AU  - Stanković, Marija
AU  - Mangano, Katia
AU  - Travali, Salvatore
AU  - Donia, Marco
AU  - Fagone, Paolo
AU  - Zocca, Mai-Britt
AU  - Al-Abed, Yousef
AU  - McCubrey, James A.
AU  - Nicoletti, Ferdinando
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/548
AB  - We have examined the influence of the nitric oxide (NO)modified anti-inflammatory drug (S, R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.
PB  - Amer Soc Pharmacology Experimental Therapeutics, Bethesda
T2  - Molecular Pharmacology
T1  - Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells
EP  - 710
IS  - 4
SP  - 700
VL  - 82
DO  - 10.1124/mol.112.077842
ER  - 

@article{
author = "Mojić, Marija and Mijatović, Sanja and Maksimović-Ivanić, Danijela and Miljković, Djordje and Stošić-Grujičić, Stanislava and Stanković, Marija and Mangano, Katia and Travali, Salvatore and Donia, Marco and Fagone, Paolo and Zocca, Mai-Britt and Al-Abed, Yousef and McCubrey, James A. and Nicoletti, Ferdinando",
year = "2012",
abstract = "We have examined the influence of the nitric oxide (NO)modified anti-inflammatory drug (S, R)-3-phenyl-4,5-dihydro-5-isoxasole acetic acid (VGX-1027) named GIT-27NO or the NO-modified antiviral drug saquinavir (Saq) named Saq-NO on two colon cancer cell lines, mouse CT26CL25 and human HCT116. The effects of the drugs on cell viability, apoptosis, proliferation, and metastatic potential were analyzed. The release of NO and oxygen and nitrogen species was also determined. The efficacy of the drugs was evaluated in vivo in BALB/c mice injected with CT26CL25 cells. Both agents suppressed the growth of colon cancer cells in vitro and reduced tumor volume in syngeneic BALB/c mice. However, their mechanisms of action were different because GIT-27NO released larger amounts of nitrite than Saq-NO in cell cultures and its antitumor action depended on the intracellular NO release inside the cells. On the contrary, Saq-NO released barely detectable amounts of NO and its antitumor action was NO-independent. In fact, cotreatment with an NO-peroxynitrite scavenger revealed that GIT-27NO but not Saq-NO acts through peroxynitrite-mediated cell destruction. At the cellular level, GIT-27NO prevalently induced proapoptotic signals followed by caspase-dependent apoptosis. In contrast, Saq-NO blocked cell proliferation, changed the adhesive, migratory, and invasive properties of the cells, and decreased metastatic potential in vivo. In conclusion, differences in NO release and oxidative stress generation between GIT-27NO and Saq-NO resulted in different mechanisms that caused cell death.",
publisher = "Amer Soc Pharmacology Experimental Therapeutics, Bethesda",
journal = "Molecular Pharmacology",
title = "Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells",
pages = "710-700",
number = "4",
volume = "82",
doi = "10.1124/mol.112.077842"
}

Mojić, M., Mijatović, S., Maksimović-Ivanić, D., Miljković, D., Stošić-Grujičić, S., Stanković, M., Mangano, K., Travali, S., Donia, M., Fagone, P., Zocca, M., Al-Abed, Y., McCubrey, J. A.,& Nicoletti, F.. (2012). Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells. in Molecular Pharmacology
Amer Soc Pharmacology Experimental Therapeutics, Bethesda., 82(4), 700-710.
https://doi.org/10.1124/mol.112.077842

Mojić M, Mijatović S, Maksimović-Ivanić D, Miljković D, Stošić-Grujičić S, Stanković M, Mangano K, Travali S, Donia M, Fagone P, Zocca M, Al-Abed Y, McCubrey JA, Nicoletti F. Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells. in Molecular Pharmacology. 2012;82(4):700-710.
doi:10.1124/mol.112.077842 .

Mojić, Marija, Mijatović, Sanja, Maksimović-Ivanić, Danijela, Miljković, Djordje, Stošić-Grujičić, Stanislava, Stanković, Marija, Mangano, Katia, Travali, Salvatore, Donia, Marco, Fagone, Paolo, Zocca, Mai-Britt, Al-Abed, Yousef, McCubrey, James A., Nicoletti, Ferdinando, "Therapeutic Potential of Nitric Oxide-Modified Drugs in Colon Cancer Cells" in Molecular Pharmacology, 82, no. 4 (2012):700-710,
https://doi.org/10.1124/mol.112.077842 . .

TY  - JOUR
AU  - Timotijević, Gordana
AU  - Mostarica-Stojković, Marija
AU  - Miljković, Djordje
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/558
AB  - CxCL12, also known as SDF-1 (stromal cell derived factor-1) is a small protein that belongs to the chemokine family, whose members have a crucial role in directing cell migration. CXCL12 has an essential role in neural and vascular development, hematopoiesis and in immunity. It acts through two receptors. CXCR4 and CXCR7. While the former is a classic G protein-coupled transmembrane chemokine receptor, the latter primarily function as a scavenger of CXCL12. CXCL12 has been considered as a standard proinflammatory molecule for a long time, as it attracts leukocytes to inflammatory sites and contributes to their activation. However, recent findings indicate that this chemokine has the opposite role in neuroinflammation. In this review, basic data about molecular and functional properties of CXCL12 are presented, while its role in CNS autoimmunity is addressed in details.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - International Journal of Biochemistry & Cell Biology
T1  - CXCL12: Role in neuroinflammation
EP  - 841
IS  - 6
SP  - 838
VL  - 44
DO  - 10.1016/j.biocel.2012.03.014
ER  - 

@article{
author = "Timotijević, Gordana and Mostarica-Stojković, Marija and Miljković, Djordje",
year = "2012",
abstract = "CxCL12, also known as SDF-1 (stromal cell derived factor-1) is a small protein that belongs to the chemokine family, whose members have a crucial role in directing cell migration. CXCL12 has an essential role in neural and vascular development, hematopoiesis and in immunity. It acts through two receptors. CXCR4 and CXCR7. While the former is a classic G protein-coupled transmembrane chemokine receptor, the latter primarily function as a scavenger of CXCL12. CXCL12 has been considered as a standard proinflammatory molecule for a long time, as it attracts leukocytes to inflammatory sites and contributes to their activation. However, recent findings indicate that this chemokine has the opposite role in neuroinflammation. In this review, basic data about molecular and functional properties of CXCL12 are presented, while its role in CNS autoimmunity is addressed in details.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "International Journal of Biochemistry & Cell Biology",
title = "CXCL12: Role in neuroinflammation",
pages = "841-838",
number = "6",
volume = "44",
doi = "10.1016/j.biocel.2012.03.014"
}

Timotijević, G., Mostarica-Stojković, M.,& Miljković, D.. (2012). CXCL12: Role in neuroinflammation. in International Journal of Biochemistry & Cell Biology
Pergamon-Elsevier Science Ltd, Oxford., 44(6), 838-841.
https://doi.org/10.1016/j.biocel.2012.03.014

Timotijević G, Mostarica-Stojković M, Miljković D. CXCL12: Role in neuroinflammation. in International Journal of Biochemistry & Cell Biology. 2012;44(6):838-841.
doi:10.1016/j.biocel.2012.03.014 .

Timotijević, Gordana, Mostarica-Stojković, Marija, Miljković, Djordje, "CXCL12: Role in neuroinflammation" in International Journal of Biochemistry & Cell Biology, 44, no. 6 (2012):838-841,
https://doi.org/10.1016/j.biocel.2012.03.014 . .

TY  - JOUR
AU  - Stojanović, Ivana
AU  - Saksida, Tamara
AU  - Timotijević, Gordana
AU  - Sandler, Stellan
AU  - Stošić-Grujičić, Stanislava
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/599
AB  - Although several reports suggest a potentially deleterious role of macrophage migration inhibitory factor (MIF) in type 2 diabetes (T2D) pathology, it is still unclear how this pro-inflammatory cytokine acts on pancreatic beta cells. The aim of the present study was to evaluate MIF effects on murine beta cells in the in vitro settings mimicking T2D-associated conditions. Results indicate that recombinant MIF further increased apoptosis of pancreatic islets or MIN6 cells upon exposure to palmitic acid or glucose. This was accompanied by upregulation of several pro-apoptotic molecules. Furthermore, MIF potentiated nutrient-induced islet cell dysfunction, as revealed by lower glucose oxidation rate, ATP content, and depolarized mitochondrial membrane. The final outcome was potentiation of mitochondrial apoptotic pathway. The observed upregulation of nutrient-induced islet cell dysfunction and apoptosis by MIF implicates that silencing MIF may be beneficial for maintaining integrity of endocrine pancreas in obesity-associated T2D.
PB  - Taylor & Francis Ltd, Abingdon
T2  - Growth Factors
T1  - Macrophage migration inhibitory factor (MIF) enhances palmitic acid-and glucose-induced murine beta cell dysfunction and destruction in vitro
EP  - 393
IS  - 6
SP  - 385
VL  - 30
DO  - 10.3109/08977194.2012.734506
ER  - 

@article{
author = "Stojanović, Ivana and Saksida, Tamara and Timotijević, Gordana and Sandler, Stellan and Stošić-Grujičić, Stanislava",
year = "2012",
abstract = "Although several reports suggest a potentially deleterious role of macrophage migration inhibitory factor (MIF) in type 2 diabetes (T2D) pathology, it is still unclear how this pro-inflammatory cytokine acts on pancreatic beta cells. The aim of the present study was to evaluate MIF effects on murine beta cells in the in vitro settings mimicking T2D-associated conditions. Results indicate that recombinant MIF further increased apoptosis of pancreatic islets or MIN6 cells upon exposure to palmitic acid or glucose. This was accompanied by upregulation of several pro-apoptotic molecules. Furthermore, MIF potentiated nutrient-induced islet cell dysfunction, as revealed by lower glucose oxidation rate, ATP content, and depolarized mitochondrial membrane. The final outcome was potentiation of mitochondrial apoptotic pathway. The observed upregulation of nutrient-induced islet cell dysfunction and apoptosis by MIF implicates that silencing MIF may be beneficial for maintaining integrity of endocrine pancreas in obesity-associated T2D.",
publisher = "Taylor & Francis Ltd, Abingdon",
journal = "Growth Factors",
title = "Macrophage migration inhibitory factor (MIF) enhances palmitic acid-and glucose-induced murine beta cell dysfunction and destruction in vitro",
pages = "393-385",
number = "6",
volume = "30",
doi = "10.3109/08977194.2012.734506"
}

Stojanović, I., Saksida, T., Timotijević, G., Sandler, S.,& Stošić-Grujičić, S.. (2012). Macrophage migration inhibitory factor (MIF) enhances palmitic acid-and glucose-induced murine beta cell dysfunction and destruction in vitro. in Growth Factors
Taylor & Francis Ltd, Abingdon., 30(6), 385-393.
https://doi.org/10.3109/08977194.2012.734506

Stojanović I, Saksida T, Timotijević G, Sandler S, Stošić-Grujičić S. Macrophage migration inhibitory factor (MIF) enhances palmitic acid-and glucose-induced murine beta cell dysfunction and destruction in vitro. in Growth Factors. 2012;30(6):385-393.
doi:10.3109/08977194.2012.734506 .

Stojanović, Ivana, Saksida, Tamara, Timotijević, Gordana, Sandler, Stellan, Stošić-Grujičić, Stanislava, "Macrophage migration inhibitory factor (MIF) enhances palmitic acid-and glucose-induced murine beta cell dysfunction and destruction in vitro" in Growth Factors, 30, no. 6 (2012):385-393,
https://doi.org/10.3109/08977194.2012.734506 . .

TY  - JOUR
AU  - Radović, J.
AU  - Maksimović-Ivanić, Danijela
AU  - Timotijević, Gordana
AU  - Popadić, S.
AU  - Ramić, Z.
AU  - Trajković, V.
AU  - Miljković, D.
AU  - Stošić-Grujičić, Stanislava
AU  - Mijatović, S.
PY  - 2012
UR  - https://imagine.imgge.bg.ac.rs/handle/123456789/550
AB  - Intrinsic characteristics of melanoma cells such as expression of inducible nitric oxide synthase (iNOS), redox status, and activity of signaling pathways involved in proliferation, differentiation and cell death define the response of the cells to the diverse treatments. In this context we compared the effectiveness of herbal antaquinone aloe emodin (AE) against mouse B16 melanoma and human A375, different in initial activity of ERK1/2, constitutive iNOS expression and basal level of reactive oxygen species (ROS). Both cell lines are sensitive to AE treatment. However, while the agent induces differentiation of B16 cells toward melanocytes, in A375 cells promoted massive apoptosis. Differentiation of B16 cells, characterized by enhanced melanin production and tyrosinase activity, was mediated by H2O2 production synchronized with rapid p53 accumulation and enhanced expression of cyclins D1 and D3. Caspase mediated apoptosis triggered in A375 cells was accompanied with Bcl-2 but not iNOS down-regulation. In addition, opposite regulation of Akt-ERK1/2 axis in AE treated B16 and A375 cells correlated with different outcome of the treatment. However, AE in a dose-dependent manner rescued both B16 and A375 cells from doxorubicin- or paclitaxel-induced killing. These data indicate that caution is warranted when AE is administrated to the patients with conventional chemotherapy.
PB  - Pergamon-Elsevier Science Ltd, Oxford
T2  - Food and Chemical Toxicology
T1  - Cell-type dependent response of melanoma cells to aloe emodin
EP  - 3189
IS  - 9
SP  - 3181
VL  - 50
DO  - 10.1016/j.fct.2012.05.047
ER  - 

@article{
author = "Radović, J. and Maksimović-Ivanić, Danijela and Timotijević, Gordana and Popadić, S. and Ramić, Z. and Trajković, V. and Miljković, D. and Stošić-Grujičić, Stanislava and Mijatović, S.",
year = "2012",
abstract = "Intrinsic characteristics of melanoma cells such as expression of inducible nitric oxide synthase (iNOS), redox status, and activity of signaling pathways involved in proliferation, differentiation and cell death define the response of the cells to the diverse treatments. In this context we compared the effectiveness of herbal antaquinone aloe emodin (AE) against mouse B16 melanoma and human A375, different in initial activity of ERK1/2, constitutive iNOS expression and basal level of reactive oxygen species (ROS). Both cell lines are sensitive to AE treatment. However, while the agent induces differentiation of B16 cells toward melanocytes, in A375 cells promoted massive apoptosis. Differentiation of B16 cells, characterized by enhanced melanin production and tyrosinase activity, was mediated by H2O2 production synchronized with rapid p53 accumulation and enhanced expression of cyclins D1 and D3. Caspase mediated apoptosis triggered in A375 cells was accompanied with Bcl-2 but not iNOS down-regulation. In addition, opposite regulation of Akt-ERK1/2 axis in AE treated B16 and A375 cells correlated with different outcome of the treatment. However, AE in a dose-dependent manner rescued both B16 and A375 cells from doxorubicin- or paclitaxel-induced killing. These data indicate that caution is warranted when AE is administrated to the patients with conventional chemotherapy.",
publisher = "Pergamon-Elsevier Science Ltd, Oxford",
journal = "Food and Chemical Toxicology",
title = "Cell-type dependent response of melanoma cells to aloe emodin",
pages = "3189-3181",
number = "9",
volume = "50",
doi = "10.1016/j.fct.2012.05.047"
}

Radović, J., Maksimović-Ivanić, D., Timotijević, G., Popadić, S., Ramić, Z., Trajković, V., Miljković, D., Stošić-Grujičić, S.,& Mijatović, S.. (2012). Cell-type dependent response of melanoma cells to aloe emodin. in Food and Chemical Toxicology
Pergamon-Elsevier Science Ltd, Oxford., 50(9), 3181-3189.
https://doi.org/10.1016/j.fct.2012.05.047

Radović J, Maksimović-Ivanić D, Timotijević G, Popadić S, Ramić Z, Trajković V, Miljković D, Stošić-Grujičić S, Mijatović S. Cell-type dependent response of melanoma cells to aloe emodin. in Food and Chemical Toxicology. 2012;50(9):3181-3189.
doi:10.1016/j.fct.2012.05.047 .

Radović, J., Maksimović-Ivanić, Danijela, Timotijević, Gordana, Popadić, S., Ramić, Z., Trajković, V., Miljković, D., Stošić-Grujičić, Stanislava, Mijatović, S., "Cell-type dependent response of melanoma cells to aloe emodin" in Food and Chemical Toxicology, 50, no. 9 (2012):3181-3189,
https://doi.org/10.1016/j.fct.2012.05.047 . .