TY  - JOUR
AU  - Mijatović, Sanja
AU  - Maksimović-Ivanić, Danijela
AU  - Radović, Julijana
AU  - Miljković, Đorđe
AU  - Harhaji-Trajković, Ljubica
AU  - Vučković, Olivera
AU  - Stošić-Grujičić, Stanislava
AU  - Mostarica Stojković, Marija
AU  - Trajković, Vladimir
PY  - 2005
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3840
AB  - The effect of aloe emodin (AE), a herbal anthraquinone derivative, on the rat C6 glioma cell line was investigated. In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-kappaB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells.
PB  - New York: Springer
T2  - Cellular and Molecular Life Sciences
T1  - Anti-glioma action of aloe emodin: the role of ERK inhibition
VL  - 62
DO  - 10.1007/s00018-005-4425-8
SP  - 589
EP  - 598
ER  - 

@article{
author = "Mijatović, Sanja and Maksimović-Ivanić, Danijela and Radović, Julijana and Miljković, Đorđe and Harhaji-Trajković, Ljubica and Vučković, Olivera and Stošić-Grujičić, Stanislava and Mostarica Stojković, Marija and Trajković, Vladimir",
year = "2005",
abstract = "The effect of aloe emodin (AE), a herbal anthraquinone derivative, on the rat C6 glioma cell line was investigated. In addition to cell cycle block and caspasedependent apoptosis, AE led to the formation of intracytoplasmic acidic vesicles indicative for autophagic cell death. Moreover, differentiation of surviving cells toward the astrocytic lineage was confirmed by typical morphological changes and increased expression of glial fibrillary acidic protein (GFAP). AE did not affect the activation of mitogen-activated protein kinase p38, Jun-N-terminal kinase, or transcription factor NF-kappaB, but markedly inhibited the activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in C6 cells. A selective inhibitor of ERK activation, PD98059, mimicked the effects of AE on glioma cell morphology and GFAP expression, but failed to induce either apoptosis or autophagy. Taken together, these results indicate that the anti-glioma action of AE involves ERK-independent induction of both apoptosis and autophagy, as well as ERK inhibition-mediated differentiation of glioma cells.",
publisher = "New York: Springer",
journal = "Cellular and Molecular Life Sciences",
title = "Anti-glioma action of aloe emodin: the role of ERK inhibition",
volume = "62",
doi = "10.1007/s00018-005-4425-8",
pages = "589-598"
}

Mijatović, S., Maksimović-Ivanić, D., Radović, J., Miljković, Đ., Harhaji-Trajković, L., Vučković, O., Stošić-Grujičić, S., Mostarica Stojković, M.,& Trajković, V.. (2005). Anti-glioma action of aloe emodin: the role of ERK inhibition. in Cellular and Molecular Life Sciences
New York: Springer., 62, 589-598.
https://doi.org/10.1007/s00018-005-4425-8

Mijatović S, Maksimović-Ivanić D, Radović J, Miljković Đ, Harhaji-Trajković L, Vučković O, Stošić-Grujičić S, Mostarica Stojković M, Trajković V. Anti-glioma action of aloe emodin: the role of ERK inhibition. in Cellular and Molecular Life Sciences. 2005;62:589-598.
doi:10.1007/s00018-005-4425-8 .

Mijatović, Sanja, Maksimović-Ivanić, Danijela, Radović, Julijana, Miljković, Đorđe, Harhaji-Trajković, Ljubica, Vučković, Olivera, Stošić-Grujičić, Stanislava, Mostarica Stojković, Marija, Trajković, Vladimir, "Anti-glioma action of aloe emodin: the role of ERK inhibition" in Cellular and Molecular Life Sciences, 62 (2005):589-598,
https://doi.org/10.1007/s00018-005-4425-8 . .

TY  - JOUR
AU  - Drulović, Jelena
AU  - Popadić, Dušan
AU  - Mesaroš, Šarlota
AU  - Dujmović, Irena
AU  - Stojanović, Ivana D.
AU  - Miljković, Djordje
AU  - Stojsavljević, Nebojša
AU  - Pravica, Vera
AU  - Pekmezović, Tatjana
AU  - Bogdanović, Gradimir
AU  - Jarebinski, Mirjana
AU  - Mostarica Stojković, Marija
PY  - 2003
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5924
AB  - Tumor necrosis factor (TNF) alpha has been considered the prototypic cytopathogenic cytokine in multiple sclerosis (MS), but recently this cytokine has been shown to possess significant anti-inflammatory and neuroprotective effects in demyelinating diseases. It has been reported that the TNFalpha -308 polymorphism influences levels of TNFalpha production, and that the rare allele, TNF2, is associated with high TNFalpha production. We investigated the TNFalpha -308 polymorphism in 143 unrelated Serbian patients with MS and 123 ethnically matched, healthy individuals using the allele-specific restriction fragment length polymorphism polymerase chain reaction technique. The frequency of the TNF2 allele was significantly decreased in MS patients (14%) in comparison with controls (24%; p = 0.044). The TNF2 allele had no influence on disease behavior, since it was not associated with the course and severity of MS in this group of patients. The result suggests that in the Serbian population polymorphism at position -308 of TNFalpha or at an adjacent locus might have a role in MS susceptibility.
PB  - Basel: Krager AG
T2  - European Neurology
T1  - Decreased Frequency of the Tumor Necrosis Factor α –308 Allele in Serbian Patients with Multiple Sclerosis
IS  - 1
VL  - 50
DO  - 10.1159/000070855
SP  - 25
EP  - 29
ER  - 

@article{
author = "Drulović, Jelena and Popadić, Dušan and Mesaroš, Šarlota and Dujmović, Irena and Stojanović, Ivana D. and Miljković, Djordje and Stojsavljević, Nebojša and Pravica, Vera and Pekmezović, Tatjana and Bogdanović, Gradimir and Jarebinski, Mirjana and Mostarica Stojković, Marija",
year = "2003",
abstract = "Tumor necrosis factor (TNF) alpha has been considered the prototypic cytopathogenic cytokine in multiple sclerosis (MS), but recently this cytokine has been shown to possess significant anti-inflammatory and neuroprotective effects in demyelinating diseases. It has been reported that the TNFalpha -308 polymorphism influences levels of TNFalpha production, and that the rare allele, TNF2, is associated with high TNFalpha production. We investigated the TNFalpha -308 polymorphism in 143 unrelated Serbian patients with MS and 123 ethnically matched, healthy individuals using the allele-specific restriction fragment length polymorphism polymerase chain reaction technique. The frequency of the TNF2 allele was significantly decreased in MS patients (14%) in comparison with controls (24%; p = 0.044). The TNF2 allele had no influence on disease behavior, since it was not associated with the course and severity of MS in this group of patients. The result suggests that in the Serbian population polymorphism at position -308 of TNFalpha or at an adjacent locus might have a role in MS susceptibility.",
publisher = "Basel: Krager AG",
journal = "European Neurology",
title = "Decreased Frequency of the Tumor Necrosis Factor α –308 Allele in Serbian Patients with Multiple Sclerosis",
number = "1",
volume = "50",
doi = "10.1159/000070855",
pages = "25-29"
}

Drulović, J., Popadić, D., Mesaroš, Š., Dujmović, I., Stojanović, I. D., Miljković, D., Stojsavljević, N., Pravica, V., Pekmezović, T., Bogdanović, G., Jarebinski, M.,& Mostarica Stojković, M.. (2003). Decreased Frequency of the Tumor Necrosis Factor α –308 Allele in Serbian Patients with Multiple Sclerosis. in European Neurology
Basel: Krager AG., 50(1), 25-29.
https://doi.org/10.1159/000070855

Drulović J, Popadić D, Mesaroš Š, Dujmović I, Stojanović ID, Miljković D, Stojsavljević N, Pravica V, Pekmezović T, Bogdanović G, Jarebinski M, Mostarica Stojković M. Decreased Frequency of the Tumor Necrosis Factor α –308 Allele in Serbian Patients with Multiple Sclerosis. in European Neurology. 2003;50(1):25-29.
doi:10.1159/000070855 .

Drulović, Jelena, Popadić, Dušan, Mesaroš, Šarlota, Dujmović, Irena, Stojanović, Ivana D., Miljković, Djordje, Stojsavljević, Nebojša, Pravica, Vera, Pekmezović, Tatjana, Bogdanović, Gradimir, Jarebinski, Mirjana, Mostarica Stojković, Marija, "Decreased Frequency of the Tumor Necrosis Factor α –308 Allele in Serbian Patients with Multiple Sclerosis" in European Neurology, 50, no. 1 (2003):25-29,
https://doi.org/10.1159/000070855 . .

TY  - JOUR
AU  - Trajković, Vladimir
AU  - Stošić-Grujičić, Stanislava
AU  - Samardzić, Tatjana
AU  - Marković, Miloš
AU  - Miljković, Đorđe
AU  - Ramić, Zorica
AU  - Mostarica Stojković, Marija
PY  - 2001
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5997
AB  - The effect of interleukin-17 (IL-17) on production of nitric oxide (NO) in rodent astrocytes was investigated. While IL-17 by itself did not induce NO production, it caused a dose-dependent enhancement of IFN-gamma-triggered NO synthesis in both mouse and rat primary astrocytes. In contrast, IL-17 was unable to stimulate NO synthesis in either murine or rat macrophages. IFN-gamma-triggered expression of mRNA for iNOS, but not for its transcription factor interferon regulatory factor-1 (IRF-1), was markedly elevated in IL-17-treated astrocytes. The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580. While IL-17 stimulated both IL-1beta and IL-6 production in astrocytes, only IL-1 was partly responsible for IL-17-induced NO release. Finally, IL-17 synergized with exogenous IL-1beta and TNF-alpha for astrocyte NO production. Having in mind a well-known neurotoxic action of NO, these results suggest a possible role for IL-17 in the inflammatory diseases of the CNS.
PB  - Amsterdam: Elsevier
T2  - Journal of Neuroimmunology
T1  - Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes
IS  - 2
VL  - 119
DO  - 10.1016/s0165-5728(01)00391-5
SP  - 183
EP  - 191
ER  - 

@article{
author = "Trajković, Vladimir and Stošić-Grujičić, Stanislava and Samardzić, Tatjana and Marković, Miloš and Miljković, Đorđe and Ramić, Zorica and Mostarica Stojković, Marija",
year = "2001",
abstract = "The effect of interleukin-17 (IL-17) on production of nitric oxide (NO) in rodent astrocytes was investigated. While IL-17 by itself did not induce NO production, it caused a dose-dependent enhancement of IFN-gamma-triggered NO synthesis in both mouse and rat primary astrocytes. In contrast, IL-17 was unable to stimulate NO synthesis in either murine or rat macrophages. IFN-gamma-triggered expression of mRNA for iNOS, but not for its transcription factor interferon regulatory factor-1 (IRF-1), was markedly elevated in IL-17-treated astrocytes. The induction of iNOS mRNA by IL-17 in IFN-gamma-pretreated astrocytes was abolished by antagonists of nuclear factor-kappaB (NF-kappaB) activation--a proteasome inhibitor MG132 and an antioxidant agent PDTC, as well as with specific p38 MAP kinase inhibitor SB203580. While IL-17 stimulated both IL-1beta and IL-6 production in astrocytes, only IL-1 was partly responsible for IL-17-induced NO release. Finally, IL-17 synergized with exogenous IL-1beta and TNF-alpha for astrocyte NO production. Having in mind a well-known neurotoxic action of NO, these results suggest a possible role for IL-17 in the inflammatory diseases of the CNS.",
publisher = "Amsterdam: Elsevier",
journal = "Journal of Neuroimmunology",
title = "Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes",
number = "2",
volume = "119",
doi = "10.1016/s0165-5728(01)00391-5",
pages = "183-191"
}

Trajković, V., Stošić-Grujičić, S., Samardzić, T., Marković, M., Miljković, Đ., Ramić, Z.,& Mostarica Stojković, M.. (2001). Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes. in Journal of Neuroimmunology
Amsterdam: Elsevier., 119(2), 183-191.
https://doi.org/10.1016/s0165-5728(01)00391-5

Trajković V, Stošić-Grujičić S, Samardzić T, Marković M, Miljković Đ, Ramić Z, Mostarica Stojković M. Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes. in Journal of Neuroimmunology. 2001;119(2):183-191.
doi:10.1016/s0165-5728(01)00391-5 .

Trajković, Vladimir, Stošić-Grujičić, Stanislava, Samardzić, Tatjana, Marković, Miloš, Miljković, Đorđe, Ramić, Zorica, Mostarica Stojković, Marija, "Interleukin-17 stimulates inducible nitric oxide synthase activation in rodent astrocytes" in Journal of Neuroimmunology, 119, no. 2 (2001):183-191,
https://doi.org/10.1016/s0165-5728(01)00391-5 . .