Milenković, Marina

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  • Milenković, Marina (2)
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Author's Bibliography

Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.

Paunović, Verica; Vukovič Petrović, Irena; Milenković, Marina; Janjetović, Kristina; Pravica, Vera; Dujmović, Irena; Milošević, Emina; Martinović, Vanja; Mesaroš, Šarlota; Drulović, Jelena; Trajković, Vladimir

(2018)

TY  - JOUR
AU  - Paunović, Verica
AU  - Vukovič Petrović, Irena
AU  - Milenković, Marina
AU  - Janjetović, Kristina
AU  - Pravica, Vera
AU  - Dujmović, Irena
AU  - Milošević, Emina
AU  - Martinović, Vanja
AU  - Mesaroš, Šarlota
AU  - Drulović, Jelena
AU  - Trajković, Vladimir
PY  - 2018
UR  - http://www.jni-journal.com/article/S0165-5728(17)30538-6/abstract
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3014
AB  - Autophagy, a process of controlled self-digestion which regulates cell homeostasis, is involved in innate and adaptive immunity. We investigated the expression of autophagy genes and autophagic activity in distinct lymphocyte populations in treatment-naive MS patients. The mRNA and protein levels of autophagy-related (ATG)5, required for autophagosome formation, were increased in CD4+and CD4-T cells, but not B cells of MS patients compared to control subjects. The expression of other investigated autophagy genes, as well as the autophagic activity, did not significantly differ between the two groups. ATG5 mRNA levels in CD4+T cells from MS patients were positively correlated with those of the proinflammatory cytokine tumor necrosis factor. These data suggest that autophagy-independent increase in ATG5 expression might be associated with the proinflammatory capacity of T cells in multiple sclerosis.
T2  - Journal of Neuroimmunology
T1  - Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.
VL  - 319
DO  - 10.1016/j.jneuroim.2018.03.001
SP  - 100
EP  - 105
ER  - 
@article{
author = "Paunović, Verica and Vukovič Petrović, Irena and Milenković, Marina and Janjetović, Kristina and Pravica, Vera and Dujmović, Irena and Milošević, Emina and Martinović, Vanja and Mesaroš, Šarlota and Drulović, Jelena and Trajković, Vladimir",
year = "2018",
abstract = "Autophagy, a process of controlled self-digestion which regulates cell homeostasis, is involved in innate and adaptive immunity. We investigated the expression of autophagy genes and autophagic activity in distinct lymphocyte populations in treatment-naive MS patients. The mRNA and protein levels of autophagy-related (ATG)5, required for autophagosome formation, were increased in CD4+and CD4-T cells, but not B cells of MS patients compared to control subjects. The expression of other investigated autophagy genes, as well as the autophagic activity, did not significantly differ between the two groups. ATG5 mRNA levels in CD4+T cells from MS patients were positively correlated with those of the proinflammatory cytokine tumor necrosis factor. These data suggest that autophagy-independent increase in ATG5 expression might be associated with the proinflammatory capacity of T cells in multiple sclerosis.",
journal = "Journal of Neuroimmunology",
title = "Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.",
volume = "319",
doi = "10.1016/j.jneuroim.2018.03.001",
pages = "100-105"
}
Paunović, V., Vukovič Petrović, I., Milenković, M., Janjetović, K., Pravica, V., Dujmović, I., Milošević, E., Martinović, V., Mesaroš, Š., Drulović, J.,& Trajković, V.. (2018). Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.. in Journal of Neuroimmunology, 319, 100-105.
https://doi.org/10.1016/j.jneuroim.2018.03.001
Paunović V, Vukovič Petrović I, Milenković M, Janjetović K, Pravica V, Dujmović I, Milošević E, Martinović V, Mesaroš Š, Drulović J, Trajković V. Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients.. in Journal of Neuroimmunology. 2018;319:100-105.
doi:10.1016/j.jneuroim.2018.03.001 .
Paunović, Verica, Vukovič Petrović, Irena, Milenković, Marina, Janjetović, Kristina, Pravica, Vera, Dujmović, Irena, Milošević, Emina, Martinović, Vanja, Mesaroš, Šarlota, Drulović, Jelena, Trajković, Vladimir, "Autophagy-independent increase of ATG5 expression in T cells of multiple sclerosis patients." in Journal of Neuroimmunology, 319 (2018):100-105,
https://doi.org/10.1016/j.jneuroim.2018.03.001 . .
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mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells

Tovilović-Kovačević, Gordana; Ristić, Biljana; Šiljić, Marina; Nikolić, Valentina; Kravić-Stevović, Tamara; Dulović, Marija; Milenković, Marina; Knežević, Aleksandra; Bošnjak, Mihajlo; Bumbaširević, Vladimir; Stanojević, Maja; Trajković, Vladimir

(Elsevier Masson SAS, 2013)

TY  - JOUR
AU  - Tovilović-Kovačević, Gordana
AU  - Ristić, Biljana
AU  - Šiljić, Marina
AU  - Nikolić, Valentina
AU  - Kravić-Stevović, Tamara
AU  - Dulović, Marija
AU  - Milenković, Marina
AU  - Knežević, Aleksandra
AU  - Bošnjak, Mihajlo
AU  - Bumbaširević, Vladimir
AU  - Stanojević, Maja
AU  - Trajković, Vladimir
PY  - 2013
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6345
AB  - We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3b, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response.
PB  - Elsevier Masson SAS
T2  - Microbes and Infection
T1  - mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells
IS  - 8-9
VL  - 15
DO  - 10.1016/j.micinf.2013.04.012
SP  - 615
EP  - 624
ER  - 
@article{
author = "Tovilović-Kovačević, Gordana and Ristić, Biljana and Šiljić, Marina and Nikolić, Valentina and Kravić-Stevović, Tamara and Dulović, Marija and Milenković, Marina and Knežević, Aleksandra and Bošnjak, Mihajlo and Bumbaširević, Vladimir and Stanojević, Maja and Trajković, Vladimir",
year = "2013",
abstract = "We investigated the role of autophagy, a stress-inducible lysosomal self-digestion of cellular components, in modulation of herpes simplex virus type 1 (HSV-1)-triggered death of U251 human glioma cells. HSV-1 caused apoptotic death in U251 cells, characterized by phosphatidylserine externalization, caspase activation and DNA fragmentation. HSV-1-induced apoptosis was associated with the induction of autophagic response, as confirmed by the conversion of cytosolic LC3-I to autophagosome-associated LC3-II, increase in intracellular acidification, presence of autophagic vesicles, and increase in proteolysis of the selective autophagic target p62. HSV-1-triggered autophagy was not associated with the significant increase in the expression of proautophagic protein beclin-1 or downregulation of the major autophagy suppressor mammalian target of rapamycin (mTOR). Moreover, the phosphorylation of mTOR and its direct substrate p70 S6 kinase was augmented by HSV-1 infection, while the mTOR stimulator Akt and inhibitor AMPK-activated protein kinase (AMPK) were accordingly activated and suppressed, respectively. An shRNA-mediated knockdown of the autophagy-essential LC3b, as well as pharmacological inhibition of autophagy with bafilomycin A1 or 3-methyladenine, markedly accelerated apoptotic changes and ensuing cell death in HSV-1-infected glioma cells. These data indicate that AMPK/Akt/mTOR-independent autophagy could prolong survival of HSV-1-infected U251 glioma cells by counteracting the coinciding apoptotic response.",
publisher = "Elsevier Masson SAS",
journal = "Microbes and Infection",
title = "mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells",
number = "8-9",
volume = "15",
doi = "10.1016/j.micinf.2013.04.012",
pages = "615-624"
}
Tovilović-Kovačević, G., Ristić, B., Šiljić, M., Nikolić, V., Kravić-Stevović, T., Dulović, M., Milenković, M., Knežević, A., Bošnjak, M., Bumbaširević, V., Stanojević, M.,& Trajković, V.. (2013). mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells. in Microbes and Infection
Elsevier Masson SAS., 15(8-9), 615-624.
https://doi.org/10.1016/j.micinf.2013.04.012
Tovilović-Kovačević G, Ristić B, Šiljić M, Nikolić V, Kravić-Stevović T, Dulović M, Milenković M, Knežević A, Bošnjak M, Bumbaširević V, Stanojević M, Trajković V. mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells. in Microbes and Infection. 2013;15(8-9):615-624.
doi:10.1016/j.micinf.2013.04.012 .
Tovilović-Kovačević, Gordana, Ristić, Biljana, Šiljić, Marina, Nikolić, Valentina, Kravić-Stevović, Tamara, Dulović, Marija, Milenković, Marina, Knežević, Aleksandra, Bošnjak, Mihajlo, Bumbaširević, Vladimir, Stanojević, Maja, Trajković, Vladimir, "mTOR-independent autophagy counteracts apoptosis in herpes simplex virus type 1-infected U251 glioma cells" in Microbes and Infection, 15, no. 8-9 (2013):615-624,
https://doi.org/10.1016/j.micinf.2013.04.012 . .
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