TY  - CONF
AU  - Misirkić Marjanović, Maja
AU  - Vučićević, Ljubica
AU  - Ćirić, Darko
AU  - Martinović, Tamara
AU  - Jovanović, Maja
AU  - Isaković, Aleksandra
AU  - Marković, Ivanka
AU  - Trajković, Vladimir
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6661
AB  - We investigated the role of autophagy in glutamate excitotoxicity during nutrient deprivation in vitro. Lack of serum, amino acids, and glucose markedly increased the sensitivity of SH-SY5Y human neuroblastoma cell line to glutamate-induced excitotoxic necrosis. Glutamate suppressed starvation-triggered autophagic response, as confirmed by diminished intracellular acidification, lower LC3 punctuation and conversion of LC3I to autophagosome associated LC3II, reduced levels of autophagy activators beclin-1 and ATG5, increased levels of the selective autophagic target NBR1, and reduced appearance of autophagic vesicles observed by transmission electron microscopy. Glutamate reduced starvation-triggered phosphorylation of the intracellular energy sensor AMP-activated protein kinase (AMPK), without affecting the activity of mammalian target of rapamycin complex1 as a major negative regulator of autophagy. Similar results were shown on PC12 cells, which are often exploited as a model for excitotoxicity. We also detected reduced mRNA expression of autophagy transcription factors FOXO3 and ATF4, as well as molecules involved in autophagy initiation (ULK1, ATG13, FIP200), autophagosome nucleation/elongation (ATG14, beclin 1, ATG5, ATG12), and the autophagy cargo delivery to autophagosmes (SQSTM1/p62). Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate dependent autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.
PB  - Nordic Autophagy Society
C3  - 3rd Nordic Autophagy Society (NAS) Conference; 2019 May 22-24; Utrecht, Nederlands
T1  - Glutamate-mediated autophagy inhibition intensifies excitotoxic death of nutrient-deprived SH-SY5Y neuroblastoma cells
SP  - 34
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_6661
ER  - 

@conference{
author = "Misirkić Marjanović, Maja and Vučićević, Ljubica and Ćirić, Darko and Martinović, Tamara and Jovanović, Maja and Isaković, Aleksandra and Marković, Ivanka and Trajković, Vladimir",
year = "2019",
abstract = "We investigated the role of autophagy in glutamate excitotoxicity during nutrient deprivation in vitro. Lack of serum, amino acids, and glucose markedly increased the sensitivity of SH-SY5Y human neuroblastoma cell line to glutamate-induced excitotoxic necrosis. Glutamate suppressed starvation-triggered autophagic response, as confirmed by diminished intracellular acidification, lower LC3 punctuation and conversion of LC3I to autophagosome associated LC3II, reduced levels of autophagy activators beclin-1 and ATG5, increased levels of the selective autophagic target NBR1, and reduced appearance of autophagic vesicles observed by transmission electron microscopy. Glutamate reduced starvation-triggered phosphorylation of the intracellular energy sensor AMP-activated protein kinase (AMPK), without affecting the activity of mammalian target of rapamycin complex1 as a major negative regulator of autophagy. Similar results were shown on PC12 cells, which are often exploited as a model for excitotoxicity. We also detected reduced mRNA expression of autophagy transcription factors FOXO3 and ATF4, as well as molecules involved in autophagy initiation (ULK1, ATG13, FIP200), autophagosome nucleation/elongation (ATG14, beclin 1, ATG5, ATG12), and the autophagy cargo delivery to autophagosmes (SQSTM1/p62). Genetic or pharmacological AMPK activation by AMPK overexpression or metformin, reduced the sensitivity of nutrient-deprived SH-SY5Y cells to glutamate dependent autophagy is involved in glutamate-mediated excitotoxicity during nutrient deprivation in vitro.",
publisher = "Nordic Autophagy Society",
journal = "3rd Nordic Autophagy Society (NAS) Conference; 2019 May 22-24; Utrecht, Nederlands",
title = "Glutamate-mediated autophagy inhibition intensifies excitotoxic death of nutrient-deprived SH-SY5Y neuroblastoma cells",
pages = "34",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_6661"
}

Misirkić Marjanović, M., Vučićević, L., Ćirić, D., Martinović, T., Jovanović, M., Isaković, A., Marković, I.,& Trajković, V.. (2019). Glutamate-mediated autophagy inhibition intensifies excitotoxic death of nutrient-deprived SH-SY5Y neuroblastoma cells. in 3rd Nordic Autophagy Society (NAS) Conference; 2019 May 22-24; Utrecht, Nederlands
Nordic Autophagy Society., 34.
https://hdl.handle.net/21.15107/rcub_ibiss_6661

Misirkić Marjanović M, Vučićević L, Ćirić D, Martinović T, Jovanović M, Isaković A, Marković I, Trajković V. Glutamate-mediated autophagy inhibition intensifies excitotoxic death of nutrient-deprived SH-SY5Y neuroblastoma cells. in 3rd Nordic Autophagy Society (NAS) Conference; 2019 May 22-24; Utrecht, Nederlands. 2019;:34.
https://hdl.handle.net/21.15107/rcub_ibiss_6661 .

Misirkić Marjanović, Maja, Vučićević, Ljubica, Ćirić, Darko, Martinović, Tamara, Jovanović, Maja, Isaković, Aleksandra, Marković, Ivanka, Trajković, Vladimir, "Glutamate-mediated autophagy inhibition intensifies excitotoxic death of nutrient-deprived SH-SY5Y neuroblastoma cells" in 3rd Nordic Autophagy Society (NAS) Conference; 2019 May 22-24; Utrecht, Nederlands (2019):34,
https://hdl.handle.net/21.15107/rcub_ibiss_6661 .

TY  - JOUR
AU  - Harhaji-Trajković, Ljubica
AU  - Isaković, Aleksandra
AU  - Zogović, Nevena
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Nikolić, Nadežda
AU  - Vranješ-Đurić, Sanja
AU  - Marković, Ivanka
AU  - Trajković, Vladimir
PY  - 2007
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/6544
AB  - Using the rat glioma cell line C6 and the human glioma cell line U251, we demonstrate the multiple mechanisms underlying the in vitro anticancer effects of the C(60) fullerene water suspension (nano-C(60) or nC(60)) produced by solvent exchange method. Nano-C(60) in a dose-dependent manner reduced the tumor cell numbers after 24 h of incubation. The observed antiglioma action of nC(60) at high concentration (1 microg/ml) was due to a reactive oxygen species-mediated necrotic cell damage that was partly dependent on oxidative stress-induced activation of extracellular signal-regulated kinase (ERK). On the other hand, low-dose nC(60) (0.25 microg/ml) did not induce either necrotic or apoptotic cell death, but caused oxidative stress/ERK-independent cell cycle block in G(2)/M phase and subsequent inhibition of tumor cell proliferation. Treatment with either high-dose or low-dose nC(60) caused the appearance of acidified intracytoplasmic vesicles indicative of autophagy, but only the antiglioma effect of low-dose nC(60) was significantly attenuated by inhibiting autophagy with bafilomycin A1. Importantly, primary rat astrocytes were less sensitive than their transformed counterparts to a cytostatic action of low-dose nC(60). These data provide grounds for further development of nC(60) as an anticancer agent.
PB  - Elsevier BV
T2  - European Journal of Pharmacology
T1  - Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene
IS  - 1-3
VL  - 568
DO  - 10.1016/j.ejphar.2007.04.041
SP  - 89
EP  - 98
ER  - 

@article{
author = "Harhaji-Trajković, Ljubica and Isaković, Aleksandra and Zogović, Nevena and Marković, Zoran and Todorović-Marković, Biljana and Nikolić, Nadežda and Vranješ-Đurić, Sanja and Marković, Ivanka and Trajković, Vladimir",
year = "2007",
abstract = "Using the rat glioma cell line C6 and the human glioma cell line U251, we demonstrate the multiple mechanisms underlying the in vitro anticancer effects of the C(60) fullerene water suspension (nano-C(60) or nC(60)) produced by solvent exchange method. Nano-C(60) in a dose-dependent manner reduced the tumor cell numbers after 24 h of incubation. The observed antiglioma action of nC(60) at high concentration (1 microg/ml) was due to a reactive oxygen species-mediated necrotic cell damage that was partly dependent on oxidative stress-induced activation of extracellular signal-regulated kinase (ERK). On the other hand, low-dose nC(60) (0.25 microg/ml) did not induce either necrotic or apoptotic cell death, but caused oxidative stress/ERK-independent cell cycle block in G(2)/M phase and subsequent inhibition of tumor cell proliferation. Treatment with either high-dose or low-dose nC(60) caused the appearance of acidified intracytoplasmic vesicles indicative of autophagy, but only the antiglioma effect of low-dose nC(60) was significantly attenuated by inhibiting autophagy with bafilomycin A1. Importantly, primary rat astrocytes were less sensitive than their transformed counterparts to a cytostatic action of low-dose nC(60). These data provide grounds for further development of nC(60) as an anticancer agent.",
publisher = "Elsevier BV",
journal = "European Journal of Pharmacology",
title = "Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene",
number = "1-3",
volume = "568",
doi = "10.1016/j.ejphar.2007.04.041",
pages = "89-98"
}

Harhaji-Trajković, L., Isaković, A., Zogović, N., Marković, Z., Todorović-Marković, B., Nikolić, N., Vranješ-Đurić, S., Marković, I.,& Trajković, V.. (2007). Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene. in European Journal of Pharmacology
Elsevier BV., 568(1-3), 89-98.
https://doi.org/10.1016/j.ejphar.2007.04.041

Harhaji-Trajković L, Isaković A, Zogović N, Marković Z, Todorović-Marković B, Nikolić N, Vranješ-Đurić S, Marković I, Trajković V. Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene. in European Journal of Pharmacology. 2007;568(1-3):89-98.
doi:10.1016/j.ejphar.2007.04.041 .

Harhaji-Trajković, Ljubica, Isaković, Aleksandra, Zogović, Nevena, Marković, Zoran, Todorović-Marković, Biljana, Nikolić, Nadežda, Vranješ-Đurić, Sanja, Marković, Ivanka, Trajković, Vladimir, "Multiple mechanisms underlying the anticancer action of nanocrystalline fullerene" in European Journal of Pharmacology, 568, no. 1-3 (2007):89-98,
https://doi.org/10.1016/j.ejphar.2007.04.041 . .