TY  - JOUR
AU  - Miljković, Đorđe
AU  - Marković, Miloš
AU  - Trajković, Vladimir
PY  - 2004
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6012
AB  - The focus of this review is the influence of an immunosuppressive xenobiotic drug mycophenolic acid on the induction of nitric oxide production in various cell types. The potential therapeutic significance of the cell-specific fine-tuning of nitric oxide release by mycophenolic acid, as well as the mechanisms behind the drug action are discussed.
PB  - Bentham Science Publishers Ltd.
T2  - Mini-Reviews in Medicinal Chemistry
T1  - Inducible nitric oxide synthase inhibition by mycophenolic acid
IS  - 7
VL  - 4
DO  - 10.2174/1389557043403585
SP  - 741
EP  - 746
ER  - 

@article{
author = "Miljković, Đorđe and Marković, Miloš and Trajković, Vladimir",
year = "2004",
abstract = "The focus of this review is the influence of an immunosuppressive xenobiotic drug mycophenolic acid on the induction of nitric oxide production in various cell types. The potential therapeutic significance of the cell-specific fine-tuning of nitric oxide release by mycophenolic acid, as well as the mechanisms behind the drug action are discussed.",
publisher = "Bentham Science Publishers Ltd.",
journal = "Mini-Reviews in Medicinal Chemistry",
title = "Inducible nitric oxide synthase inhibition by mycophenolic acid",
number = "7",
volume = "4",
doi = "10.2174/1389557043403585",
pages = "741-746"
}

Miljković, Đ., Marković, M.,& Trajković, V.. (2004). Inducible nitric oxide synthase inhibition by mycophenolic acid. in Mini-Reviews in Medicinal Chemistry
Bentham Science Publishers Ltd.., 4(7), 741-746.
https://doi.org/10.2174/1389557043403585

Miljković Đ, Marković M, Trajković V. Inducible nitric oxide synthase inhibition by mycophenolic acid. in Mini-Reviews in Medicinal Chemistry. 2004;4(7):741-746.
doi:10.2174/1389557043403585 .

Miljković, Đorđe, Marković, Miloš, Trajković, Vladimir, "Inducible nitric oxide synthase inhibition by mycophenolic acid" in Mini-Reviews in Medicinal Chemistry, 4, no. 7 (2004):741-746,
https://doi.org/10.2174/1389557043403585 . .

TY  - JOUR
AU  - Marković, Miloš
AU  - Miljković, Đorđe
AU  - Trajković, Vladimir
PY  - 2003
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6002
AB  - Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). While being a major microbicidal and tumoricidal molecule, iNOS-derived NO has also been implicated in tissue destruction, as well as in regulation of inflammatory/immune cell function in various disorders associated with excessive inflammation. A feasible way for cAMP-dependent therapeutic control of inflammation, including iNOS-mediated NO synthesis, could involve the administration of drugs that block the enzymatic activity of cAMP-degrading phosphodiesterases (PDE). Indeed, cAMP-elevating PDE inhibitors can influence iNOS activation in different cell types in vitro, and their potent anti-inflammatory effects in experimental disease models and clinical studies were frequently accompanied with profound modulation of NO production. A set of conflicting data has been generated over the years, ranging from strong suppression to marked enhancement of NO release by cAMP-increasing PDE inhibitors, depending on cell-type, iNOS stimuli, and/or the agents used. The present review summarizes the data on iNOS modulation by cAMP-elevating PDE inhibitors and possible mechanisms behind it, speculating on its contribution to the therapeutic effects of these drugs.
PB  - Bentham Science Publishers Ltd.
T2  - Current Drug Targets - Inflammation and Allergy
T1  - Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors
IS  - 1
VL  - 2
DO  - 10.2174/1568010033344471
SP  - 63
EP  - 67
ER  - 

@article{
author = "Marković, Miloš and Miljković, Đorđe and Trajković, Vladimir",
year = "2003",
abstract = "Among the numerous genes controlled by cyclic adenosine monophosphate (cAMP)/protein kinase A signalling machinery is the gene encoding the inducible nitric oxide synthase (iNOS), an enzyme catalyzing the synthesis of a highly reactive free radical nitric oxide (NO). While being a major microbicidal and tumoricidal molecule, iNOS-derived NO has also been implicated in tissue destruction, as well as in regulation of inflammatory/immune cell function in various disorders associated with excessive inflammation. A feasible way for cAMP-dependent therapeutic control of inflammation, including iNOS-mediated NO synthesis, could involve the administration of drugs that block the enzymatic activity of cAMP-degrading phosphodiesterases (PDE). Indeed, cAMP-elevating PDE inhibitors can influence iNOS activation in different cell types in vitro, and their potent anti-inflammatory effects in experimental disease models and clinical studies were frequently accompanied with profound modulation of NO production. A set of conflicting data has been generated over the years, ranging from strong suppression to marked enhancement of NO release by cAMP-increasing PDE inhibitors, depending on cell-type, iNOS stimuli, and/or the agents used. The present review summarizes the data on iNOS modulation by cAMP-elevating PDE inhibitors and possible mechanisms behind it, speculating on its contribution to the therapeutic effects of these drugs.",
publisher = "Bentham Science Publishers Ltd.",
journal = "Current Drug Targets - Inflammation and Allergy",
title = "Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors",
number = "1",
volume = "2",
doi = "10.2174/1568010033344471",
pages = "63-67"
}

Marković, M., Miljković, Đ.,& Trajković, V.. (2003). Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors. in Current Drug Targets - Inflammation and Allergy
Bentham Science Publishers Ltd.., 2(1), 63-67.
https://doi.org/10.2174/1568010033344471

Marković M, Miljković Đ, Trajković V. Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors. in Current Drug Targets - Inflammation and Allergy. 2003;2(1):63-67.
doi:10.2174/1568010033344471 .

Marković, Miloš, Miljković, Đorđe, Trajković, Vladimir, "Regulation of inducible nitric oxide synthase by cAMP-elevating phospho-diesterase inhibitors" in Current Drug Targets - Inflammation and Allergy, 2, no. 1 (2003):63-67,
https://doi.org/10.2174/1568010033344471 . .

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 . .

TY  - JOUR
AU  - Trajković, Vladimir
AU  - Marković, Miloš
AU  - Samardzić, Tatjana
AU  - Miljković, Đorđe
AU  - Popadić, Dušan
AU  - Mostarica Stojković, Marija
PY  - 2001
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5996
AB  - Because the neurotoxic effects of the antifungal drug amphotericin B
(AMB) closely resemble those ascribed to the highly reactive gaseous free radical nitric
oxide (NO), we investigated the effect of AMB on NO production in rodent astrocytes.
AMB caused a dose-dependent increase of NO generation in interferon-g (IFN-g)-stimulated rat and mouse astrocytes, as well as in IFN-g 1 tumor necrosis factor-a (TNFa)-activated rat astrocytoma cell line C6. Treatment of rat astrocytes with AMB markedly potentiated IFN-g-triggered expression of mRNA for iNOS, but not for its
transcription factor IRF-1. The activation of transcription factor NF-kB was apparently
required for AMB-induced iNOS mRNA expression, as the latter was abolished by
NF-kB inhibitors: pyrrolidine dithiocarbamate and MG132. AMB-mediated enhancement of astrocyte NO production was partly dependent on endogenous IL-1, as shown by
partial inhibition of AMB effect with IL-1 receptor antagonist. IFN-g 1 AMB treatment
led to reduction of astrocyte mitochondrial respiration (measured by MTT assay) that
has been completely reverted by selective iNOS inhibitor aminoguanidine. AMB toxicity
toward IFN-g-stimulated astrocytes was dependent on both AMB and NO action, since
AMB and NO-releasing substance SNP synergized in inducing astrocyte mitochondrial
dysfunction. These results suggest that the enhancement of cytokine-induced iNOS
activation in astrocytes and the subsequent release of high amounts of NO might be at
least partly responsible for AMB neurotoxicity.
PB  - Hoboken: Wiley
T2  - Glia
T1  - Amphotericin B Potentiates the Activation of Inducible Nitric Oxide Synthase and Causes Nitric OxideDependent Mitochondrial Dysfunction in Cytokine-Treated Rodent Astrocytes
IS  - 3
VL  - 35
DO  - 10.1002/glia.1083
SP  - 180
EP  - 188
ER  - 

@article{
author = "Trajković, Vladimir and Marković, Miloš and Samardzić, Tatjana and Miljković, Đorđe and Popadić, Dušan and Mostarica Stojković, Marija",
year = "2001",
abstract = "Because the neurotoxic effects of the antifungal drug amphotericin B
(AMB) closely resemble those ascribed to the highly reactive gaseous free radical nitric
oxide (NO), we investigated the effect of AMB on NO production in rodent astrocytes.
AMB caused a dose-dependent increase of NO generation in interferon-g (IFN-g)-stimulated rat and mouse astrocytes, as well as in IFN-g 1 tumor necrosis factor-a (TNFa)-activated rat astrocytoma cell line C6. Treatment of rat astrocytes with AMB markedly potentiated IFN-g-triggered expression of mRNA for iNOS, but not for its
transcription factor IRF-1. The activation of transcription factor NF-kB was apparently
required for AMB-induced iNOS mRNA expression, as the latter was abolished by
NF-kB inhibitors: pyrrolidine dithiocarbamate and MG132. AMB-mediated enhancement of astrocyte NO production was partly dependent on endogenous IL-1, as shown by
partial inhibition of AMB effect with IL-1 receptor antagonist. IFN-g 1 AMB treatment
led to reduction of astrocyte mitochondrial respiration (measured by MTT assay) that
has been completely reverted by selective iNOS inhibitor aminoguanidine. AMB toxicity
toward IFN-g-stimulated astrocytes was dependent on both AMB and NO action, since
AMB and NO-releasing substance SNP synergized in inducing astrocyte mitochondrial
dysfunction. These results suggest that the enhancement of cytokine-induced iNOS
activation in astrocytes and the subsequent release of high amounts of NO might be at
least partly responsible for AMB neurotoxicity.",
publisher = "Hoboken: Wiley",
journal = "Glia",
title = "Amphotericin B Potentiates the Activation of Inducible Nitric Oxide Synthase and Causes Nitric OxideDependent Mitochondrial Dysfunction in Cytokine-Treated Rodent Astrocytes",
number = "3",
volume = "35",
doi = "10.1002/glia.1083",
pages = "180-188"
}

Trajković, V., Marković, M., Samardzić, T., Miljković, Đ., Popadić, D.,& Mostarica Stojković, M.. (2001). Amphotericin B Potentiates the Activation of Inducible Nitric Oxide Synthase and Causes Nitric OxideDependent Mitochondrial Dysfunction in Cytokine-Treated Rodent Astrocytes. in Glia
Hoboken: Wiley., 35(3), 180-188.
https://doi.org/10.1002/glia.1083

Trajković V, Marković M, Samardzić T, Miljković Đ, Popadić D, Mostarica Stojković M. Amphotericin B Potentiates the Activation of Inducible Nitric Oxide Synthase and Causes Nitric OxideDependent Mitochondrial Dysfunction in Cytokine-Treated Rodent Astrocytes. in Glia. 2001;35(3):180-188.
doi:10.1002/glia.1083 .

Trajković, Vladimir, Marković, Miloš, Samardzić, Tatjana, Miljković, Đorđe, Popadić, Dušan, Mostarica Stojković, Marija, "Amphotericin B Potentiates the Activation of Inducible Nitric Oxide Synthase and Causes Nitric OxideDependent Mitochondrial Dysfunction in Cytokine-Treated Rodent Astrocytes" in Glia, 35, no. 3 (2001):180-188,
https://doi.org/10.1002/glia.1083 . .