TY  - CONF
AU  - Tasić, Jelena
AU  - Vidičević Novaković, Sašenka
AU  - Stanojević, Željka
AU  - Paunović, Verica
AU  - Petričević, Saša
AU  - Martinović, Tamara
AU  - Kravić-Stevović, Tamara
AU  - Ćirić, Darko
AU  - Marković, Zoran J.
AU  - Isaković, Aleksandra
AU  - Trajković, Vladimir
PY  - 2023
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/11057
AB  - Background: Experimental autoimmune encephalomyelitis (EAE) is one of the most studied model of neuroinflammation, used to test immunomodulatory and antiinflammatory drugs. Graphene quantum dots (GQD) are oval graphite twodimensional sheets with a diameter <100 nm, one carbon atom thickness, with potential applications in biomedicine. Objective: To investigate the potential protective effect of GQD in EAE model. Methods: Female DA rats were immunized with spinal cord homogenate and Freund’s complete adjuvant. GQD treatment (10 mg/kg, ip) was administrated during the inductive, effector and both phases of a disease. MAP kinase (MAPK) and Akt activity in popliteal lymph nodes (PLN) and CNS was determined by western blot. Quantitative PCR and flow cytometry were used to examine the expression of proinflammatory cytokines and specific transcription factors while infiltration of GQD in cells/tissues was detected by transmission electron microscopy. GQD antiinflamatory/direct cytoprotective effect was analyzed on oligodendrocyte and neuron cell cultures by MTT assay. Data were analized by Mann Whitney test (p<0.05 was considered as statistical significant difference). Results: GQD administration, in all phases of EAE, significantly reduced clinical score of a disease. Clinical improvement correlates with increase in activity of ERK, p38 and Akt that is followed by reduction of Th1 cell response in PLN and infiltrated spinal coard T cells. Due to its capacity to infiltrate cells and tissues, GQD exhibits direct cytoprotective effect on CNS. Additionaly, GQD reduced the expression of proinflammatory cytokines in ConA stimulated lymphocytes. Conclusion: GQD alleviate EAE, through direct cytoprotective effect on CNS and inhibition of Th1 cell response.
PB  - Belgrade : Serbian Neuroscience Society
C3  - 8th Congress of Serbian neuroscience society with international participation : the book of abstracts; 31 May – 2 June; Belgrade
T1  - Graphene Quantum Dots show protective effect in animal model of neuroinflammation
SP  - 114
UR  - https://hdl.handle.net/21.15107/rcub_vinar_11057
ER  - 

@conference{
author = "Tasić, Jelena and Vidičević Novaković, Sašenka and Stanojević, Željka and Paunović, Verica and Petričević, Saša and Martinović, Tamara and Kravić-Stevović, Tamara and Ćirić, Darko and Marković, Zoran J. and Isaković, Aleksandra and Trajković, Vladimir",
year = "2023",
abstract = "Background: Experimental autoimmune encephalomyelitis (EAE) is one of the most studied model of neuroinflammation, used to test immunomodulatory and antiinflammatory drugs. Graphene quantum dots (GQD) are oval graphite twodimensional sheets with a diameter <100 nm, one carbon atom thickness, with potential applications in biomedicine. Objective: To investigate the potential protective effect of GQD in EAE model. Methods: Female DA rats were immunized with spinal cord homogenate and Freund’s complete adjuvant. GQD treatment (10 mg/kg, ip) was administrated during the inductive, effector and both phases of a disease. MAP kinase (MAPK) and Akt activity in popliteal lymph nodes (PLN) and CNS was determined by western blot. Quantitative PCR and flow cytometry were used to examine the expression of proinflammatory cytokines and specific transcription factors while infiltration of GQD in cells/tissues was detected by transmission electron microscopy. GQD antiinflamatory/direct cytoprotective effect was analyzed on oligodendrocyte and neuron cell cultures by MTT assay. Data were analized by Mann Whitney test (p<0.05 was considered as statistical significant difference). Results: GQD administration, in all phases of EAE, significantly reduced clinical score of a disease. Clinical improvement correlates with increase in activity of ERK, p38 and Akt that is followed by reduction of Th1 cell response in PLN and infiltrated spinal coard T cells. Due to its capacity to infiltrate cells and tissues, GQD exhibits direct cytoprotective effect on CNS. Additionaly, GQD reduced the expression of proinflammatory cytokines in ConA stimulated lymphocytes. Conclusion: GQD alleviate EAE, through direct cytoprotective effect on CNS and inhibition of Th1 cell response.",
publisher = "Belgrade : Serbian Neuroscience Society",
journal = "8th Congress of Serbian neuroscience society with international participation : the book of abstracts; 31 May – 2 June; Belgrade",
title = "Graphene Quantum Dots show protective effect in animal model of neuroinflammation",
pages = "114",
url = "https://hdl.handle.net/21.15107/rcub_vinar_11057"
}

Tasić, J., Vidičević Novaković, S., Stanojević, Ž., Paunović, V., Petričević, S., Martinović, T., Kravić-Stevović, T., Ćirić, D., Marković, Z. J., Isaković, A.,& Trajković, V.. (2023). Graphene Quantum Dots show protective effect in animal model of neuroinflammation. in 8th Congress of Serbian neuroscience society with international participation : the book of abstracts; 31 May – 2 June; Belgrade
Belgrade : Serbian Neuroscience Society., 114.
https://hdl.handle.net/21.15107/rcub_vinar_11057

Tasić J, Vidičević Novaković S, Stanojević Ž, Paunović V, Petričević S, Martinović T, Kravić-Stevović T, Ćirić D, Marković ZJ, Isaković A, Trajković V. Graphene Quantum Dots show protective effect in animal model of neuroinflammation. in 8th Congress of Serbian neuroscience society with international participation : the book of abstracts; 31 May – 2 June; Belgrade. 2023;:114.
https://hdl.handle.net/21.15107/rcub_vinar_11057 .

Tasić, Jelena, Vidičević Novaković, Sašenka, Stanojević, Željka, Paunović, Verica, Petričević, Saša, Martinović, Tamara, Kravić-Stevović, Tamara, Ćirić, Darko, Marković, Zoran J., Isaković, Aleksandra, Trajković, Vladimir, "Graphene Quantum Dots show protective effect in animal model of neuroinflammation" in 8th Congress of Serbian neuroscience society with international participation : the book of abstracts; 31 May – 2 June; Belgrade (2023):114,
https://hdl.handle.net/21.15107/rcub_vinar_11057 .

TY  - JOUR
AU  - Krunić, Matija
AU  - Ristić, Biljana
AU  - Bošnjak, Mihajlo
AU  - Paunović, Verica
AU  - Tovilović-Kovačević, Gordana
AU  - Zogović, Nevena
AU  - Mirčić, Aleksandar
AU  - Marković, Zoran
AU  - Todorović-Marković, Biljana
AU  - Jovanović, Svetlana P.
AU  - Kleut, Duška
AU  - Mojović, Miloš
AU  - Nakarada, Đura
AU  - Marković, Olivera
AU  - Vuković, Irena
AU  - Harhaji-Trajković, Ljubica
AU  - Trajković, Vladimir S.
PY  - 2021
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9980
AB  - We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP).GQD reduced SNP cytotoxicity by preventing mitochondrial depolarization, caspase-2 activation, and subsequent apoptotic death. Although GQD diminished the levels of nitric oxide (NO) in SNP-exposed cells, NO scavengers displayed only a slight protective effect, suggesting that NO quenching was not the main protective mechanism of GQD. GQD also reduced SNP-triggered increase in the intracellular levels of hydroxyl radical (•OH), superoxide anion (O2•- ), and lipid peroxidation. Nonselective antioxidants, •OH scavenging, and iron chelators, but not superoxide dismutase, mimicked GQD cytoprotective activity, indicating that GQD protect cells by neutralizing •OH generated in the presence of SNP-released iron. Cellular internalization of GQD was required for optimal protection, since a removal of extracellular GQD by extensive washing only partly diminished their protective effect. Moreover, GQD cooperated with SNP to induce autophagy, as confirmed by the inhibition of autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic beclin-1 and LC3-II, formation of autophagic vesicles, and degradation of autophagic target p62. The antioxidant activity of GQD was not involved in autophagy induction, as antioxidants N-acetylcysteine and dimethyl sulfoxide failed to stimulate autophagy in SNP-exposed cells. Pharmacological inhibitors of early (wortmannin, 3-methyladenine) or late stages of autophagy (NH4Cl) efficiently reduced the protective effect of GQD. Therefore, the ability of GQD to prevent the in vitro neurotoxicity of SNP depends on both •OH/NO scavenging and induction of cytoprotective autophagy.
T2  - Free Radical Biology and Medicine
T1  - Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death
VL  - 177
SP  - 167
EP  - 180
DO  - 10.1016/j.freeradbiomed.2021.10.025
ER  - 

@article{
author = "Krunić, Matija and Ristić, Biljana and Bošnjak, Mihajlo and Paunović, Verica and Tovilović-Kovačević, Gordana and Zogović, Nevena and Mirčić, Aleksandar and Marković, Zoran and Todorović-Marković, Biljana and Jovanović, Svetlana P. and Kleut, Duška and Mojović, Miloš and Nakarada, Đura and Marković, Olivera and Vuković, Irena and Harhaji-Trajković, Ljubica and Trajković, Vladimir S.",
year = "2021",
abstract = "We investigated the ability of graphene quantum dot (GQD) nanoparticles to protect SH-SY5Y human neuroblastoma cells from oxidative/nitrosative stress induced by iron-nitrosyl complex sodium nitroprusside (SNP).GQD reduced SNP cytotoxicity by preventing mitochondrial depolarization, caspase-2 activation, and subsequent apoptotic death. Although GQD diminished the levels of nitric oxide (NO) in SNP-exposed cells, NO scavengers displayed only a slight protective effect, suggesting that NO quenching was not the main protective mechanism of GQD. GQD also reduced SNP-triggered increase in the intracellular levels of hydroxyl radical (•OH), superoxide anion (O2•- ), and lipid peroxidation. Nonselective antioxidants, •OH scavenging, and iron chelators, but not superoxide dismutase, mimicked GQD cytoprotective activity, indicating that GQD protect cells by neutralizing •OH generated in the presence of SNP-released iron. Cellular internalization of GQD was required for optimal protection, since a removal of extracellular GQD by extensive washing only partly diminished their protective effect. Moreover, GQD cooperated with SNP to induce autophagy, as confirmed by the inhibition of autophagylimiting Akt/PRAS40/mTOR signaling and increase in autophagy gene transcription, protein levels of proautophagic beclin-1 and LC3-II, formation of autophagic vesicles, and degradation of autophagic target p62. The antioxidant activity of GQD was not involved in autophagy induction, as antioxidants N-acetylcysteine and dimethyl sulfoxide failed to stimulate autophagy in SNP-exposed cells. Pharmacological inhibitors of early (wortmannin, 3-methyladenine) or late stages of autophagy (NH4Cl) efficiently reduced the protective effect of GQD. Therefore, the ability of GQD to prevent the in vitro neurotoxicity of SNP depends on both •OH/NO scavenging and induction of cytoprotective autophagy.",
journal = "Free Radical Biology and Medicine",
title = "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death",
volume = "177",
pages = "167-180",
doi = "10.1016/j.freeradbiomed.2021.10.025"
}

Krunić, M., Ristić, B., Bošnjak, M., Paunović, V., Tovilović-Kovačević, G., Zogović, N., Mirčić, A., Marković, Z., Todorović-Marković, B., Jovanović, S. P., Kleut, D., Mojović, M., Nakarada, Đ., Marković, O., Vuković, I., Harhaji-Trajković, L.,& Trajković, V. S.. (2021). Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine, 177, 167-180.
https://doi.org/10.1016/j.freeradbiomed.2021.10.025

Krunić M, Ristić B, Bošnjak M, Paunović V, Tovilović-Kovačević G, Zogović N, Mirčić A, Marković Z, Todorović-Marković B, Jovanović SP, Kleut D, Mojović M, Nakarada Đ, Marković O, Vuković I, Harhaji-Trajković L, Trajković VS. Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death. in Free Radical Biology and Medicine. 2021;177:167-180.
doi:10.1016/j.freeradbiomed.2021.10.025 .

Krunić, Matija, Ristić, Biljana, Bošnjak, Mihajlo, Paunović, Verica, Tovilović-Kovačević, Gordana, Zogović, Nevena, Mirčić, Aleksandar, Marković, Zoran, Todorović-Marković, Biljana, Jovanović, Svetlana P., Kleut, Duška, Mojović, Miloš, Nakarada, Đura, Marković, Olivera, Vuković, Irena, Harhaji-Trajković, Ljubica, Trajković, Vladimir S., "Graphene quantum dot antioxidant and proautophagic actions protect SH-SY5Y neuroblastoma cells from oxidative stress-mediated apoptotic death" in Free Radical Biology and Medicine, 177 (2021):167-180,
https://doi.org/10.1016/j.freeradbiomed.2021.10.025 . .

TY  - JOUR
AU  - Tošić, Jelena
AU  - Stanojević, Željka
AU  - Vidičević, Sašenka
AU  - Isaković, Aleksandra J.
AU  - Ćirić, Darko
AU  - Martinović, Tamara
AU  - Kravić-Stevović, Tamara K.
AU  - Bumbaširević, Vladimir Ž.
AU  - Paunović, Verica G.
AU  - Jovanović, Svetlana P.
AU  - Todorović-Marković, Biljana
AU  - Marković, Zoran M.
AU  - Danko, Martin
AU  - Mičušik, Matej
AU  - Spitalsky, Zdenko
AU  - Trajković, Vladimir S.
PY  - 2019
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0028390818308621
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8015
AB  - We investigated the therapeutic capacity of nano-sized graphene sheets, called graphene quantum dots (GQD), in experimental autoimmune encephalomyelitis (EAE), an animal model of immune-mediated central nervous system (CNS) damage. Intraperitoneally administered GQD (10 mg/kg/day) accumulated in the lymph node and CNS cells of Dark Agouti rats in which EAE was induced by immunization with spinal cord homogenate in complete Freund's adjuvant. GQD significantly reduced clinical signs of EAE when applied throughout the course of the disease (day 0–32), while the protection was less pronounced if the treatment was limited to the induction (day 0–7 post-immunization) or effector (from day 8 onwards) phase of the disease. GQD treatment diminished immune infiltration, demyelination, axonal damage, and apoptotic death in the CNS of EAE animals. GQD also reduced the numbers of interferon-γ-expressing T helper (Th)1 cells, as well as the expression of Th1 transcription factor T-bet and proinflammatory cytokines tumor necrosis factor, interleukin-1, and granulocyte-macrophage colony-stimulating factor in the lymph nodes and CNS immune infitrates. The protective effect of GQD in EAE was associated with the activation of p38 and p42/44 mitogen-activated protein kinases (MAPK) and Akt in the lymph nodes and/or CNS. Finally, GQD protected oligodendrocytes and neurons from T cell-mediated damage in the in vitro conditions. Collectively, these data demonstrate the ability of GQD to gain access to both immune and CNS cells during neuroinflammation, and to alleviate immune-mediated CNS damage by modulating MAPK/Akt signaling and encephalitogenic Th1 immune response. © 2018 Elsevier Ltd
T2  - Neuropharmacology
T1  - Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats
VL  - 146
SP  - 95
EP  - 108
DO  - 10.1016/j.neuropharm.2018.11.030
ER  - 

@article{
author = "Tošić, Jelena and Stanojević, Željka and Vidičević, Sašenka and Isaković, Aleksandra J. and Ćirić, Darko and Martinović, Tamara and Kravić-Stevović, Tamara K. and Bumbaširević, Vladimir Ž. and Paunović, Verica G. and Jovanović, Svetlana P. and Todorović-Marković, Biljana and Marković, Zoran M. and Danko, Martin and Mičušik, Matej and Spitalsky, Zdenko and Trajković, Vladimir S.",
year = "2019",
abstract = "We investigated the therapeutic capacity of nano-sized graphene sheets, called graphene quantum dots (GQD), in experimental autoimmune encephalomyelitis (EAE), an animal model of immune-mediated central nervous system (CNS) damage. Intraperitoneally administered GQD (10 mg/kg/day) accumulated in the lymph node and CNS cells of Dark Agouti rats in which EAE was induced by immunization with spinal cord homogenate in complete Freund's adjuvant. GQD significantly reduced clinical signs of EAE when applied throughout the course of the disease (day 0–32), while the protection was less pronounced if the treatment was limited to the induction (day 0–7 post-immunization) or effector (from day 8 onwards) phase of the disease. GQD treatment diminished immune infiltration, demyelination, axonal damage, and apoptotic death in the CNS of EAE animals. GQD also reduced the numbers of interferon-γ-expressing T helper (Th)1 cells, as well as the expression of Th1 transcription factor T-bet and proinflammatory cytokines tumor necrosis factor, interleukin-1, and granulocyte-macrophage colony-stimulating factor in the lymph nodes and CNS immune infitrates. The protective effect of GQD in EAE was associated with the activation of p38 and p42/44 mitogen-activated protein kinases (MAPK) and Akt in the lymph nodes and/or CNS. Finally, GQD protected oligodendrocytes and neurons from T cell-mediated damage in the in vitro conditions. Collectively, these data demonstrate the ability of GQD to gain access to both immune and CNS cells during neuroinflammation, and to alleviate immune-mediated CNS damage by modulating MAPK/Akt signaling and encephalitogenic Th1 immune response. © 2018 Elsevier Ltd",
journal = "Neuropharmacology",
title = "Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats",
volume = "146",
pages = "95-108",
doi = "10.1016/j.neuropharm.2018.11.030"
}

Tošić, J., Stanojević, Ž., Vidičević, S., Isaković, A. J., Ćirić, D., Martinović, T., Kravić-Stevović, T. K., Bumbaširević, V. Ž., Paunović, V. G., Jovanović, S. P., Todorović-Marković, B., Marković, Z. M., Danko, M., Mičušik, M., Spitalsky, Z.,& Trajković, V. S.. (2019). Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats. in Neuropharmacology, 146, 95-108.
https://doi.org/10.1016/j.neuropharm.2018.11.030

Tošić J, Stanojević Ž, Vidičević S, Isaković AJ, Ćirić D, Martinović T, Kravić-Stevović TK, Bumbaširević VŽ, Paunović VG, Jovanović SP, Todorović-Marković B, Marković ZM, Danko M, Mičušik M, Spitalsky Z, Trajković VS. Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats. in Neuropharmacology. 2019;146:95-108.
doi:10.1016/j.neuropharm.2018.11.030 .

Tošić, Jelena, Stanojević, Željka, Vidičević, Sašenka, Isaković, Aleksandra J., Ćirić, Darko, Martinović, Tamara, Kravić-Stevović, Tamara K., Bumbaširević, Vladimir Ž., Paunović, Verica G., Jovanović, Svetlana P., Todorović-Marković, Biljana, Marković, Zoran M., Danko, Martin, Mičušik, Matej, Spitalsky, Zdenko, Trajković, Vladimir S., "Graphene quantum dots inhibit T cell-mediated neuroinflammation in rats" in Neuropharmacology, 146 (2019):95-108,
https://doi.org/10.1016/j.neuropharm.2018.11.030 . .

TY  - CONF
AU  - Ćirić, Darko
AU  - Martinović, Tamara
AU  - Kravić-Stevović, Tamara K.
AU  - Volarević, Vladislav
AU  - Paunović, Verica G.
AU  - Marković, Zoran M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Todorović-Marković, Biljana
AU  - Bojić, Sanja
AU  - Vučićević, Ljubica
AU  - Jovanović, Svetlana P.
AU  - Arsenijević, Nebojša N.
AU  - Holclajtner-Antunović, Ivanka D.
AU  - Milosavljević, Momir
AU  - Dramićanin, Miroslav
AU  - Lukić, Miodrag L.
AU  - Trajković, Vladimir S.
AU  - Bumbaširević, Vladimir Ž.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8741
PB  - Belgrade : Serbian Academy of Sciences and Arts
C3  - Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia
T1  - Ultrastructural Analysis of Large Graphene Quantum Dots Internalization in Hepatocytes
SP  - 272
EP  - 274
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8741
ER  - 

@conference{
author = "Ćirić, Darko and Martinović, Tamara and Kravić-Stevović, Tamara K. and Volarević, Vladislav and Paunović, Verica G. and Marković, Zoran M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Todorović-Marković, Biljana and Bojić, Sanja and Vučićević, Ljubica and Jovanović, Svetlana P. and Arsenijević, Nebojša N. and Holclajtner-Antunović, Ivanka D. and Milosavljević, Momir and Dramićanin, Miroslav and Lukić, Miodrag L. and Trajković, Vladimir S. and Bumbaširević, Vladimir Ž.",
year = "2018",
publisher = "Belgrade : Serbian Academy of Sciences and Arts",
journal = "Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia",
title = "Ultrastructural Analysis of Large Graphene Quantum Dots Internalization in Hepatocytes",
pages = "272-274",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8741"
}

Ćirić, D., Martinović, T., Kravić-Stevović, T. K., Volarević, V., Paunović, V. G., Marković, Z. M., Marković-Simović, B., Misirkić-Marjanović, M., Todorović-Marković, B., Bojić, S., Vučićević, L., Jovanović, S. P., Arsenijević, N. N., Holclajtner-Antunović, I. D., Milosavljević, M., Dramićanin, M., Lukić, M. L., Trajković, V. S.,& Bumbaširević, V. Ž.. (2018). Ultrastructural Analysis of Large Graphene Quantum Dots Internalization in Hepatocytes. in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia
Belgrade : Serbian Academy of Sciences and Arts., 272-274.
https://hdl.handle.net/21.15107/rcub_vinar_8741

Ćirić D, Martinović T, Kravić-Stevović TK, Volarević V, Paunović VG, Marković ZM, Marković-Simović B, Misirkić-Marjanović M, Todorović-Marković B, Bojić S, Vučićević L, Jovanović SP, Arsenijević NN, Holclajtner-Antunović ID, Milosavljević M, Dramićanin M, Lukić ML, Trajković VS, Bumbaširević VŽ. Ultrastructural Analysis of Large Graphene Quantum Dots Internalization in Hepatocytes. in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia. 2018;:272-274.
https://hdl.handle.net/21.15107/rcub_vinar_8741 .

Ćirić, Darko, Martinović, Tamara, Kravić-Stevović, Tamara K., Volarević, Vladislav, Paunović, Verica G., Marković, Zoran M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Todorović-Marković, Biljana, Bojić, Sanja, Vučićević, Ljubica, Jovanović, Svetlana P., Arsenijević, Nebojša N., Holclajtner-Antunović, Ivanka D., Milosavljević, Momir, Dramićanin, Miroslav, Lukić, Miodrag L., Trajković, Vladimir S., Bumbaširević, Vladimir Ž., "Ultrastructural Analysis of Large Graphene Quantum Dots Internalization in Hepatocytes" in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia (2018):272-274,
https://hdl.handle.net/21.15107/rcub_vinar_8741 .

TY  - CONF
AU  - Kravić-Stevović, Tamara K.
AU  - Martinović, Tamara
AU  - Ćirić, Darko
AU  - Paunović, Verica G.
AU  - Ristić, Biljana
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Kosić, Milica
AU  - Prekodravac, Jovana
AU  - Micusik, Matej
AU  - Spitalsky, Zdeno
AU  - Trajković, Vladimir S.
AU  - Harhaji-Trajković, Ljubica M.
AU  - Bumbaširević, Vladimir Ž.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8740
PB  - Belgrade : Serbian Academy of Sciences and Arts
C3  - Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia
T1  - Transmission Electron Microscopy in Evaluation of Curcumin Nanoparticles Cellular Uptake
SP  - 266
EP  - 268
UR  - https://hdl.handle.net/21.15107/rcub_vinar_8740
ER  - 

@conference{
author = "Kravić-Stevović, Tamara K. and Martinović, Tamara and Ćirić, Darko and Paunović, Verica G. and Ristić, Biljana and Marković, Zoran M. and Todorović-Marković, Biljana and Kosić, Milica and Prekodravac, Jovana and Micusik, Matej and Spitalsky, Zdeno and Trajković, Vladimir S. and Harhaji-Trajković, Ljubica M. and Bumbaširević, Vladimir Ž.",
year = "2018",
publisher = "Belgrade : Serbian Academy of Sciences and Arts",
journal = "Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia",
title = "Transmission Electron Microscopy in Evaluation of Curcumin Nanoparticles Cellular Uptake",
pages = "266-268",
url = "https://hdl.handle.net/21.15107/rcub_vinar_8740"
}

Kravić-Stevović, T. K., Martinović, T., Ćirić, D., Paunović, V. G., Ristić, B., Marković, Z. M., Todorović-Marković, B., Kosić, M., Prekodravac, J., Micusik, M., Spitalsky, Z., Trajković, V. S., Harhaji-Trajković, L. M.,& Bumbaširević, V. Ž.. (2018). Transmission Electron Microscopy in Evaluation of Curcumin Nanoparticles Cellular Uptake. in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia
Belgrade : Serbian Academy of Sciences and Arts., 266-268.
https://hdl.handle.net/21.15107/rcub_vinar_8740

Kravić-Stevović TK, Martinović T, Ćirić D, Paunović VG, Ristić B, Marković ZM, Todorović-Marković B, Kosić M, Prekodravac J, Micusik M, Spitalsky Z, Trajković VS, Harhaji-Trajković LM, Bumbaširević VŽ. Transmission Electron Microscopy in Evaluation of Curcumin Nanoparticles Cellular Uptake. in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia. 2018;:266-268.
https://hdl.handle.net/21.15107/rcub_vinar_8740 .

Kravić-Stevović, Tamara K., Martinović, Tamara, Ćirić, Darko, Paunović, Verica G., Ristić, Biljana, Marković, Zoran M., Todorović-Marković, Biljana, Kosić, Milica, Prekodravac, Jovana, Micusik, Matej, Spitalsky, Zdeno, Trajković, Vladimir S., Harhaji-Trajković, Ljubica M., Bumbaširević, Vladimir Ž., "Transmission Electron Microscopy in Evaluation of Curcumin Nanoparticles Cellular Uptake" in Program and Book of Abstracts / First International Conference on Electron Microscopy of Nanostructures ELMINA 2018, August 27-29, 2018, Belgrade, Serbia (2018):266-268,
https://hdl.handle.net/21.15107/rcub_vinar_8740 .

TY  - CONF
AU  - Colic, M
AU  - Tomić, S.
AU  - Janjetović, Kristina D.
AU  - Mihajlovic, D
AU  - Milenković, M
AU  - Kravić-Stevović, Tamara K.
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Špitalsky, Zdenko
AU  - Mičušik, Matej
AU  - Vucevic, D
AU  - Trajković, Vladimir S.
PY  - 2018
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7750
AB  - Graphene quantum dots (GQD) are atom-thick nanodimensional carbon, very attractive for the application in theranostics due to their excellent physico-chemical and biological properties. However, their immunoregulatory properties are insufficiently investigated, especially for human immune cells. We found that non-toxic doses of GQD inhibit the production of proinflammatory and T helper (Th)1 cytokines, and augment the production of anti-inflammatory and Th2 cytokines by human peripheral blood  mononuclear cells. While unable to affect purified T cells directly, GQD impaired the differentiation and functions of monocyte-derived dendritic cells (DC), lowering  their capacity to stimulate T cell proliferation, development of Th1 and Th17 cells, and T-cell mediated cytotoxicity. Additionally, GQD-treated DC potentiated Th2  polarization, and induced suppressive CD4+CD25hiFoxp3hi regulatory T cells. After internalization in a dynamin-independent, cholesterol-dependent manner, GQD lowered the ROS generation and nuclear translocation of NF-B in DC. The activity of mammalian target of rapamycin (mTOR) was reduced by GQD, which correlated with the increase in transcription of autophagy genes and autophagic flux in DC. Genetic suppression of autophagy impaired the pro-tolerogenic effects of GQD on DC. Our results suggest that GQD-triggered autophagy promotes tolerogenic functions in monocyte-derived DC, which could be beneficial in inflammatory T-cell mediated pathologies, but also harmful in GQD-based anti-cancer therapy.
C3  - European Journal of Immunology
T1  - Graphene quantum dots induce tolerogenic properties in dendritic cells via induction of autophagy
VL  - 48
IS  - Supplement 1
SP  - 180
EP  - 181
DO  - 10.1002/eji.201871000
ER  - 

@conference{
author = "Colic, M and Tomić, S. and Janjetović, Kristina D. and Mihajlovic, D and Milenković, M and Kravić-Stevović, Tamara K. and Marković, Zoran M. and Todorović-Marković, Biljana and Špitalsky, Zdenko and Mičušik, Matej and Vucevic, D and Trajković, Vladimir S.",
year = "2018",
abstract = "Graphene quantum dots (GQD) are atom-thick nanodimensional carbon, very attractive for the application in theranostics due to their excellent physico-chemical and biological properties. However, their immunoregulatory properties are insufficiently investigated, especially for human immune cells. We found that non-toxic doses of GQD inhibit the production of proinflammatory and T helper (Th)1 cytokines, and augment the production of anti-inflammatory and Th2 cytokines by human peripheral blood  mononuclear cells. While unable to affect purified T cells directly, GQD impaired the differentiation and functions of monocyte-derived dendritic cells (DC), lowering  their capacity to stimulate T cell proliferation, development of Th1 and Th17 cells, and T-cell mediated cytotoxicity. Additionally, GQD-treated DC potentiated Th2  polarization, and induced suppressive CD4+CD25hiFoxp3hi regulatory T cells. After internalization in a dynamin-independent, cholesterol-dependent manner, GQD lowered the ROS generation and nuclear translocation of NF-B in DC. The activity of mammalian target of rapamycin (mTOR) was reduced by GQD, which correlated with the increase in transcription of autophagy genes and autophagic flux in DC. Genetic suppression of autophagy impaired the pro-tolerogenic effects of GQD on DC. Our results suggest that GQD-triggered autophagy promotes tolerogenic functions in monocyte-derived DC, which could be beneficial in inflammatory T-cell mediated pathologies, but also harmful in GQD-based anti-cancer therapy.",
journal = "European Journal of Immunology",
title = "Graphene quantum dots induce tolerogenic properties in dendritic cells via induction of autophagy",
volume = "48",
number = "Supplement 1",
pages = "180-181",
doi = "10.1002/eji.201871000"
}

Colic, M., Tomić, S., Janjetović, K. D., Mihajlovic, D., Milenković, M., Kravić-Stevović, T. K., Marković, Z. M., Todorović-Marković, B., Špitalsky, Z., Mičušik, M., Vucevic, D.,& Trajković, V. S.. (2018). Graphene quantum dots induce tolerogenic properties in dendritic cells via induction of autophagy. in European Journal of Immunology, 48(Supplement 1), 180-181.
https://doi.org/10.1002/eji.201871000

Colic M, Tomić S, Janjetović KD, Mihajlovic D, Milenković M, Kravić-Stevović TK, Marković ZM, Todorović-Marković B, Špitalsky Z, Mičušik M, Vucevic D, Trajković VS. Graphene quantum dots induce tolerogenic properties in dendritic cells via induction of autophagy. in European Journal of Immunology. 2018;48(Supplement 1):180-181.
doi:10.1002/eji.201871000 .

Colic, M, Tomić, S., Janjetović, Kristina D., Mihajlovic, D, Milenković, M, Kravić-Stevović, Tamara K., Marković, Zoran M., Todorović-Marković, Biljana, Špitalsky, Zdenko, Mičušik, Matej, Vucevic, D, Trajković, Vladimir S., "Graphene quantum dots induce tolerogenic properties in dendritic cells via induction of autophagy" in European Journal of Immunology, 48, no. Supplement 1 (2018):180-181,
https://doi.org/10.1002/eji.201871000 . .

TY  - JOUR
AU  - Milutinović, Milan M.
AU  - Čanović, Petar P.
AU  - Stevanović, Dragana D.
AU  - Masnikosa, Romana
AU  - Vraneš, Milan
AU  - Tot, Aleksandar
AU  - Zarić, Milan M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Vučićević, Ljubica
AU  - Savić, Maja
AU  - Jakovljević, Vladimir Lj.
AU  - Trajković, Vladimir S.
AU  - Volarević, Vladislav
AU  - Kanjevac, Tatjana
AU  - Rilak Simović, Ana
PY  - 2018
UR  - http://pubs.acs.org/doi/10.1021/acs.organomet.8b00604
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7967
AB  - The two new heterometallic Ru(II)-tpy/ferrocene complexes [Ru(tpy)Cl2(mtefc)] (1) and [Ru(tpy)Cl2(mtpfc)] (2) (where tpy = 2,2′:6′,2′′-terpyridine, mtefc = (2-(methylthio)ethyl)ferrocene, and mtpfc = (3-(methylthio)propyl)ferrocene) have been synthesized and then characterized through elemental analysis, followed by various spectroscopic (IR, UV-vis, 1D and 2D NMR) and mass spectrometric techniques (MALDI TOF and ESI Q-TOF MS). UV-vis and fluorescence spectroscopy and viscometry were employed to study the interactions of the complexes 1 and 2 with calf thymus DNA. Both 1 and 2 expelled ethidium bromide (EB) from the EB/DNA complex (Ksv = (1.5-1.8) × 104 M-1), which suggested that the complexes intercalated into the double helix of DNA. Both complexes strongly quenched the fluorescence of tryptophan residues in serum albumin through both static and dynamic quenching. Molecular docking confirmed the intercalative mode of complex interaction with DNA. The docking results implied that 1 and 2 interacted with hydrophobic residues of albumin, particularly with those lying in the proximity of Tyr 160. We here demonstrate the high cytotoxic potential of complexes 1 and 2 against the breast cancer cells that originated either from humans (MDA-MB-231) or from mice (4T1), with apoptosis being the main mechanism of complex-induced cell death. It is worth noting that both complexes promoted activation of innate and acquired antitumor immunity, which contributed to the reduced growth and progression of mammary carcinoma in vivo. Copyright © 2018 American Chemical Society.
T2  - Organometallics
T1  - Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity
VL  - 37
IS  - 22
SP  - 4250
EP  - 4266
DO  - 10.1021/acs.organomet.8b00604
ER  - 

@article{
author = "Milutinović, Milan M. and Čanović, Petar P. and Stevanović, Dragana D. and Masnikosa, Romana and Vraneš, Milan and Tot, Aleksandar and Zarić, Milan M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Vučićević, Ljubica and Savić, Maja and Jakovljević, Vladimir Lj. and Trajković, Vladimir S. and Volarević, Vladislav and Kanjevac, Tatjana and Rilak Simović, Ana",
year = "2018",
abstract = "The two new heterometallic Ru(II)-tpy/ferrocene complexes [Ru(tpy)Cl2(mtefc)] (1) and [Ru(tpy)Cl2(mtpfc)] (2) (where tpy = 2,2′:6′,2′′-terpyridine, mtefc = (2-(methylthio)ethyl)ferrocene, and mtpfc = (3-(methylthio)propyl)ferrocene) have been synthesized and then characterized through elemental analysis, followed by various spectroscopic (IR, UV-vis, 1D and 2D NMR) and mass spectrometric techniques (MALDI TOF and ESI Q-TOF MS). UV-vis and fluorescence spectroscopy and viscometry were employed to study the interactions of the complexes 1 and 2 with calf thymus DNA. Both 1 and 2 expelled ethidium bromide (EB) from the EB/DNA complex (Ksv = (1.5-1.8) × 104 M-1), which suggested that the complexes intercalated into the double helix of DNA. Both complexes strongly quenched the fluorescence of tryptophan residues in serum albumin through both static and dynamic quenching. Molecular docking confirmed the intercalative mode of complex interaction with DNA. The docking results implied that 1 and 2 interacted with hydrophobic residues of albumin, particularly with those lying in the proximity of Tyr 160. We here demonstrate the high cytotoxic potential of complexes 1 and 2 against the breast cancer cells that originated either from humans (MDA-MB-231) or from mice (4T1), with apoptosis being the main mechanism of complex-induced cell death. It is worth noting that both complexes promoted activation of innate and acquired antitumor immunity, which contributed to the reduced growth and progression of mammary carcinoma in vivo. Copyright © 2018 American Chemical Society.",
journal = "Organometallics",
title = "Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity",
volume = "37",
number = "22",
pages = "4250-4266",
doi = "10.1021/acs.organomet.8b00604"
}

Milutinović, M. M., Čanović, P. P., Stevanović, D. D., Masnikosa, R., Vraneš, M., Tot, A., Zarić, M. M., Marković-Simović, B., Misirkić-Marjanović, M., Vučićević, L., Savić, M., Jakovljević, V. Lj., Trajković, V. S., Volarević, V., Kanjevac, T.,& Rilak Simović, A.. (2018). Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity. in Organometallics, 37(22), 4250-4266.
https://doi.org/10.1021/acs.organomet.8b00604

Milutinović MM, Čanović PP, Stevanović DD, Masnikosa R, Vraneš M, Tot A, Zarić MM, Marković-Simović B, Misirkić-Marjanović M, Vučićević L, Savić M, Jakovljević VL, Trajković VS, Volarević V, Kanjevac T, Rilak Simović A. Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity. in Organometallics. 2018;37(22):4250-4266.
doi:10.1021/acs.organomet.8b00604 .

Milutinović, Milan M., Čanović, Petar P., Stevanović, Dragana D., Masnikosa, Romana, Vraneš, Milan, Tot, Aleksandar, Zarić, Milan M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Vučićević, Ljubica, Savić, Maja, Jakovljević, Vladimir Lj., Trajković, Vladimir S., Volarević, Vladislav, Kanjevac, Tatjana, Rilak Simović, Ana, "Newly Synthesized Heteronuclear Ruthenium(II)/Ferrocene Complexes Suppress the Growth of Mammary Carcinoma in 4T1-Treated BALB/c Mice by Promoting Activation of Antitumor Immunity" in Organometallics, 37, no. 22 (2018):4250-4266,
https://doi.org/10.1021/acs.organomet.8b00604 . .

TY  - JOUR
AU  - Tomić, Sergej
AU  - Janjetović, Kristina D.
AU  - Mihajlovic, Dusan
AU  - Milenković, Marina
AU  - Kravić-Stevović, Tamara K.
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Špitalsky, Zdenko
AU  - Mičušik, Matej
AU  - Vucevic, Dragana
AU  - Colic, Miodrag
AU  - Trajković, Vladimir S.
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1782
AB  - Graphene quantum dots (GQD) are atom-thick nanodimensional carbon sheets with excellent physicochemical and biological properties; making them attractive for application in theranostics: However, their immunoregulatory properties are insufficiently investigated, especially in human primary immune cells. We found that non-toxic doses of GQD inhibit the production of proinflammatory and T helper (Th) 1 cytokines, and augment the production of anti-inflammatory and Th2 cytokines by human peripheral blood mononuclear cells. While unable to affect T cells directly, GQD impaired the differentiation and functions of monocyte-derived dendritic cells (DC), lowering their capacity to stimulate T cell proliferation, development of Thl and Th17 cells, and T-cell mediated cytotoxicity. Additionally, GQD-treated DC potentiated Th2 polarization, and induced suppressive CD4(+)CD25(high)Foxp3(+) regulatory T cells. After internalization in a dynamin-independent, cholesterol-dependent manner, GQD lowered the production of reactive oxygen species and nuclear translocation of NF-kappa B in DC. The activity of mammalian target of rapamycin (mTOR) was reduced by GQD, which correlated with the increase in transcription of autophagy genes and autophagic flux in DC. Genetic suppression of autophagy impaired the pro-tolerogenic effects of GQD on DC. Our results suggest that GQD-triggered autophagy promotes tolerogenic functions in monocyte-derived DC, which could be beneficial in inflammatory T-cell mediated pathologies, but also harmful in GQD-based anti-cancer therapy. (C) 2017 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - Graphene quantum dots suppress proinflammatory T cell responses via autophagy-dependent induction of tolerogenic dendritic cells
VL  - 146
SP  - 13
EP  - 28
DO  - 10.1016/j.biomaterials.2017.08.040
ER  - 

@article{
author = "Tomić, Sergej and Janjetović, Kristina D. and Mihajlovic, Dusan and Milenković, Marina and Kravić-Stevović, Tamara K. and Marković, Zoran M. and Todorović-Marković, Biljana and Špitalsky, Zdenko and Mičušik, Matej and Vucevic, Dragana and Colic, Miodrag and Trajković, Vladimir S.",
year = "2017",
abstract = "Graphene quantum dots (GQD) are atom-thick nanodimensional carbon sheets with excellent physicochemical and biological properties; making them attractive for application in theranostics: However, their immunoregulatory properties are insufficiently investigated, especially in human primary immune cells. We found that non-toxic doses of GQD inhibit the production of proinflammatory and T helper (Th) 1 cytokines, and augment the production of anti-inflammatory and Th2 cytokines by human peripheral blood mononuclear cells. While unable to affect T cells directly, GQD impaired the differentiation and functions of monocyte-derived dendritic cells (DC), lowering their capacity to stimulate T cell proliferation, development of Thl and Th17 cells, and T-cell mediated cytotoxicity. Additionally, GQD-treated DC potentiated Th2 polarization, and induced suppressive CD4(+)CD25(high)Foxp3(+) regulatory T cells. After internalization in a dynamin-independent, cholesterol-dependent manner, GQD lowered the production of reactive oxygen species and nuclear translocation of NF-kappa B in DC. The activity of mammalian target of rapamycin (mTOR) was reduced by GQD, which correlated with the increase in transcription of autophagy genes and autophagic flux in DC. Genetic suppression of autophagy impaired the pro-tolerogenic effects of GQD on DC. Our results suggest that GQD-triggered autophagy promotes tolerogenic functions in monocyte-derived DC, which could be beneficial in inflammatory T-cell mediated pathologies, but also harmful in GQD-based anti-cancer therapy. (C) 2017 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "Graphene quantum dots suppress proinflammatory T cell responses via autophagy-dependent induction of tolerogenic dendritic cells",
volume = "146",
pages = "13-28",
doi = "10.1016/j.biomaterials.2017.08.040"
}

Tomić, S., Janjetović, K. D., Mihajlovic, D., Milenković, M., Kravić-Stevović, T. K., Marković, Z. M., Todorović-Marković, B., Špitalsky, Z., Mičušik, M., Vucevic, D., Colic, M.,& Trajković, V. S.. (2017). Graphene quantum dots suppress proinflammatory T cell responses via autophagy-dependent induction of tolerogenic dendritic cells. in Biomaterials, 146, 13-28.
https://doi.org/10.1016/j.biomaterials.2017.08.040

Tomić S, Janjetović KD, Mihajlovic D, Milenković M, Kravić-Stevović TK, Marković ZM, Todorović-Marković B, Špitalsky Z, Mičušik M, Vucevic D, Colic M, Trajković VS. Graphene quantum dots suppress proinflammatory T cell responses via autophagy-dependent induction of tolerogenic dendritic cells. in Biomaterials. 2017;146:13-28.
doi:10.1016/j.biomaterials.2017.08.040 .

Tomić, Sergej, Janjetović, Kristina D., Mihajlovic, Dusan, Milenković, Marina, Kravić-Stevović, Tamara K., Marković, Zoran M., Todorović-Marković, Biljana, Špitalsky, Zdenko, Mičušik, Matej, Vucevic, Dragana, Colic, Miodrag, Trajković, Vladimir S., "Graphene quantum dots suppress proinflammatory T cell responses via autophagy-dependent induction of tolerogenic dendritic cells" in Biomaterials, 146 (2017):13-28,
https://doi.org/10.1016/j.biomaterials.2017.08.040 . .

TY  - JOUR
AU  - Paunović, Verica G.
AU  - Ristić, Biljana
AU  - Marković, Zoran M.
AU  - Todorović-Marković, Biljana
AU  - Kosić, Milica
AU  - Prekodravac, Jovana
AU  - Kravić-Stevović, Tamara K.
AU  - Martinović, Tamara
AU  - Mičušik, Matej
AU  - Špitalsky, Zdenko
AU  - Trajković, Vladimir S.
AU  - Harhaji-Trajković, Ljubica M.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1084
AB  - Indian spice curcumin is known for its anticancer properties, but the anticancer mechanisms of nanoparticulate curcumin have not been completely elucidated. We here investigated the in vitro anticancer effect of blue light (470 nm, 1 W)-irradiated curcumin nanoparticles prepared by tetrahydrofuran/water solvent exchange, using U251 glioma, B16 melanoma, and H460 lung cancer cells as targets. The size of curcumin nanocrystals was approximately 250 nm, while photoexcitation induced their oxidation and partial agglomeration. Although cell membrane in the absence of light was almost impermeable to curcumin nanoparticles, photoexcitation stimulated their internalization. While irradiation with blue light (1-8 min) or nanocurcumin (1.25-10 mu g/ml) alone was only marginally toxic to tumor cells, photoexcited nanocurcumin displayed a significant cytotoxicity depending both on the irradiation time and nanocurcumin concentration. Photoexcited nanocurcumin induced phosphorylation of cJun N-terminal kinase (JNK), mitochondrial depolarization, caspase-3 activation, and cleavage of poly (ADP-ribose) polymerase, indicating apoptotic cell death. Accordingly, pharmacologial inhibition of JNK and caspase activity rescued cancer cells from photoexcited nanocurcumin. On the other hand, antioxidant treatment did not reduce photocytotoxicity of nanocurcumin, arguing against the involvement of oxidative stress. By demonstrating the ability of photoexcited nanocurcumin to induce oxidative-stress independent, JNK-and caspase-dependent apoptosis, our results support its further investigation in cancer therapy.
PB  - Springer
T2  - Biomedical Microdevices
T1  - c-Jun N-terminal kinase-dependent apoptotic photocytotoxicity of solvent exchange-prepared curcumin nanoparticles
VL  - 18
IS  - 2
DO  - 10.1007/s10544-016-0062-2
ER  - 

@article{
author = "Paunović, Verica G. and Ristić, Biljana and Marković, Zoran M. and Todorović-Marković, Biljana and Kosić, Milica and Prekodravac, Jovana and Kravić-Stevović, Tamara K. and Martinović, Tamara and Mičušik, Matej and Špitalsky, Zdenko and Trajković, Vladimir S. and Harhaji-Trajković, Ljubica M.",
year = "2016",
abstract = "Indian spice curcumin is known for its anticancer properties, but the anticancer mechanisms of nanoparticulate curcumin have not been completely elucidated. We here investigated the in vitro anticancer effect of blue light (470 nm, 1 W)-irradiated curcumin nanoparticles prepared by tetrahydrofuran/water solvent exchange, using U251 glioma, B16 melanoma, and H460 lung cancer cells as targets. The size of curcumin nanocrystals was approximately 250 nm, while photoexcitation induced their oxidation and partial agglomeration. Although cell membrane in the absence of light was almost impermeable to curcumin nanoparticles, photoexcitation stimulated their internalization. While irradiation with blue light (1-8 min) or nanocurcumin (1.25-10 mu g/ml) alone was only marginally toxic to tumor cells, photoexcited nanocurcumin displayed a significant cytotoxicity depending both on the irradiation time and nanocurcumin concentration. Photoexcited nanocurcumin induced phosphorylation of cJun N-terminal kinase (JNK), mitochondrial depolarization, caspase-3 activation, and cleavage of poly (ADP-ribose) polymerase, indicating apoptotic cell death. Accordingly, pharmacologial inhibition of JNK and caspase activity rescued cancer cells from photoexcited nanocurcumin. On the other hand, antioxidant treatment did not reduce photocytotoxicity of nanocurcumin, arguing against the involvement of oxidative stress. By demonstrating the ability of photoexcited nanocurcumin to induce oxidative-stress independent, JNK-and caspase-dependent apoptosis, our results support its further investigation in cancer therapy.",
publisher = "Springer",
journal = "Biomedical Microdevices",
title = "c-Jun N-terminal kinase-dependent apoptotic photocytotoxicity of solvent exchange-prepared curcumin nanoparticles",
volume = "18",
number = "2",
doi = "10.1007/s10544-016-0062-2"
}

Paunović, V. G., Ristić, B., Marković, Z. M., Todorović-Marković, B., Kosić, M., Prekodravac, J., Kravić-Stevović, T. K., Martinović, T., Mičušik, M., Špitalsky, Z., Trajković, V. S.,& Harhaji-Trajković, L. M.. (2016). c-Jun N-terminal kinase-dependent apoptotic photocytotoxicity of solvent exchange-prepared curcumin nanoparticles. in Biomedical Microdevices
Springer., 18(2).
https://doi.org/10.1007/s10544-016-0062-2

Paunović VG, Ristić B, Marković ZM, Todorović-Marković B, Kosić M, Prekodravac J, Kravić-Stevović TK, Martinović T, Mičušik M, Špitalsky Z, Trajković VS, Harhaji-Trajković LM. c-Jun N-terminal kinase-dependent apoptotic photocytotoxicity of solvent exchange-prepared curcumin nanoparticles. in Biomedical Microdevices. 2016;18(2).
doi:10.1007/s10544-016-0062-2 .

Paunović, Verica G., Ristić, Biljana, Marković, Zoran M., Todorović-Marković, Biljana, Kosić, Milica, Prekodravac, Jovana, Kravić-Stevović, Tamara K., Martinović, Tamara, Mičušik, Matej, Špitalsky, Zdenko, Trajković, Vladimir S., Harhaji-Trajković, Ljubica M., "c-Jun N-terminal kinase-dependent apoptotic photocytotoxicity of solvent exchange-prepared curcumin nanoparticles" in Biomedical Microdevices, 18, no. 2 (2016),
https://doi.org/10.1007/s10544-016-0062-2 . .

TY  - JOUR
AU  - Hulea, Laura
AU  - Marković, Zoran M.
AU  - Topisirović, Ivan
AU  - Simmet, Thomas
AU  - Trajković, Vladimir S.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1071
AB  - Modulation of the mammalian target of rapamycin (mTOR), the principal regulator of cellular homeostasis, underlies the biological effects of engineered nanoparticles, including regulation of cell death/survival and metabolic responses. Understanding the mechanisms and biological actions of nanoparticle-mediated mTOR modulation may help in developing safe and efficient nano therapeutics to fight human disease.
T2  - Trends in Biotechnology
T1  - Biomedical Potential of mTOR Modulation by Nanoparticles
VL  - 34
IS  - 5
SP  - 349
EP  - 353
DO  - 10.1016/j.tibtech.2016.01.005
ER  - 

@article{
author = "Hulea, Laura and Marković, Zoran M. and Topisirović, Ivan and Simmet, Thomas and Trajković, Vladimir S.",
year = "2016",
abstract = "Modulation of the mammalian target of rapamycin (mTOR), the principal regulator of cellular homeostasis, underlies the biological effects of engineered nanoparticles, including regulation of cell death/survival and metabolic responses. Understanding the mechanisms and biological actions of nanoparticle-mediated mTOR modulation may help in developing safe and efficient nano therapeutics to fight human disease.",
journal = "Trends in Biotechnology",
title = "Biomedical Potential of mTOR Modulation by Nanoparticles",
volume = "34",
number = "5",
pages = "349-353",
doi = "10.1016/j.tibtech.2016.01.005"
}

Hulea, L., Marković, Z. M., Topisirović, I., Simmet, T.,& Trajković, V. S.. (2016). Biomedical Potential of mTOR Modulation by Nanoparticles. in Trends in Biotechnology, 34(5), 349-353.
https://doi.org/10.1016/j.tibtech.2016.01.005

Hulea L, Marković ZM, Topisirović I, Simmet T, Trajković VS. Biomedical Potential of mTOR Modulation by Nanoparticles. in Trends in Biotechnology. 2016;34(5):349-353.
doi:10.1016/j.tibtech.2016.01.005 .

Hulea, Laura, Marković, Zoran M., Topisirović, Ivan, Simmet, Thomas, Trajković, Vladimir S., "Biomedical Potential of mTOR Modulation by Nanoparticles" in Trends in Biotechnology, 34, no. 5 (2016):349-353,
https://doi.org/10.1016/j.tibtech.2016.01.005 . .

TY  - CONF
AU  - Tošić, Jelena
AU  - Vidičević, Sašenka
AU  - Stanojević, Željka
AU  - Paunović, Verica G.
AU  - Petricevic, S.
AU  - Martinović, Tamara
AU  - Kravić-Stevović, Tamara K.
AU  - Ćirić, Darko
AU  - Marković, Zoran M.
AU  - Isaković, Aleksandra J.
AU  - Trajković, Vladimir S.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7160
C3  - European Neuropsychopharmacology
T1  - Graphene quantum dots show protective effect on a model of experimental autoimmune encephalomyelitis
VL  - 26
SP  - S211
EP  - S212
DO  - 10.1016/S0924-977X(16)31060-4
ER  - 

@conference{
author = "Tošić, Jelena and Vidičević, Sašenka and Stanojević, Željka and Paunović, Verica G. and Petricevic, S. and Martinović, Tamara and Kravić-Stevović, Tamara K. and Ćirić, Darko and Marković, Zoran M. and Isaković, Aleksandra J. and Trajković, Vladimir S.",
year = "2016",
journal = "European Neuropsychopharmacology",
title = "Graphene quantum dots show protective effect on a model of experimental autoimmune encephalomyelitis",
volume = "26",
pages = "S211-S212",
doi = "10.1016/S0924-977X(16)31060-4"
}

Tošić, J., Vidičević, S., Stanojević, Ž., Paunović, V. G., Petricevic, S., Martinović, T., Kravić-Stevović, T. K., Ćirić, D., Marković, Z. M., Isaković, A. J.,& Trajković, V. S.. (2016). Graphene quantum dots show protective effect on a model of experimental autoimmune encephalomyelitis. in European Neuropsychopharmacology, 26, S211-S212.
https://doi.org/10.1016/S0924-977X(16)31060-4

Tošić J, Vidičević S, Stanojević Ž, Paunović VG, Petricevic S, Martinović T, Kravić-Stevović TK, Ćirić D, Marković ZM, Isaković AJ, Trajković VS. Graphene quantum dots show protective effect on a model of experimental autoimmune encephalomyelitis. in European Neuropsychopharmacology. 2016;26:S211-S212.
doi:10.1016/S0924-977X(16)31060-4 .

Tošić, Jelena, Vidičević, Sašenka, Stanojević, Željka, Paunović, Verica G., Petricevic, S., Martinović, Tamara, Kravić-Stevović, Tamara K., Ćirić, Darko, Marković, Zoran M., Isaković, Aleksandra J., Trajković, Vladimir S., "Graphene quantum dots show protective effect on a model of experimental autoimmune encephalomyelitis" in European Neuropsychopharmacology, 26 (2016):S211-S212,
https://doi.org/10.1016/S0924-977X(16)31060-4 . .

TY  - CONF
AU  - Volarevic, V.
AU  - Paunović, Verica G.
AU  - Marković, Zoran M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Todorović-Marković, Biljana
AU  - Bojic, S.
AU  - Vucicevic, L.
AU  - Jovanović, Svetlana P.
AU  - Arsenijević, Nebojša N.
AU  - Holclajtner-Antunović, Ivanka D.
AU  - Milosavljević, Momir
AU  - Dramićanin, Miroslav
AU  - Kravić-Stevović, Tamara K.
AU  - Ćirić, Darko
AU  - Lukić, M. L.
AU  - Trajković, Vladimir S.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/7082
C3  - Journal of Hepatology
T1  - Graphene Quantum Dots Attenuate Concanavalin A-Induced Hepatitis
VL  - 62
SP  - S483
EP  - S484
DO  - 10.1016/S0168-8278(15)30665-6
ER  - 

@conference{
author = "Volarevic, V. and Paunović, Verica G. and Marković, Zoran M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Todorović-Marković, Biljana and Bojic, S. and Vucicevic, L. and Jovanović, Svetlana P. and Arsenijević, Nebojša N. and Holclajtner-Antunović, Ivanka D. and Milosavljević, Momir and Dramićanin, Miroslav and Kravić-Stevović, Tamara K. and Ćirić, Darko and Lukić, M. L. and Trajković, Vladimir S.",
year = "2015",
journal = "Journal of Hepatology",
title = "Graphene Quantum Dots Attenuate Concanavalin A-Induced Hepatitis",
volume = "62",
pages = "S483-S484",
doi = "10.1016/S0168-8278(15)30665-6"
}

Volarevic, V., Paunović, V. G., Marković, Z. M., Marković-Simović, B., Misirkić-Marjanović, M., Todorović-Marković, B., Bojic, S., Vucicevic, L., Jovanović, S. P., Arsenijević, N. N., Holclajtner-Antunović, I. D., Milosavljević, M., Dramićanin, M., Kravić-Stevović, T. K., Ćirić, D., Lukić, M. L.,& Trajković, V. S.. (2015). Graphene Quantum Dots Attenuate Concanavalin A-Induced Hepatitis. in Journal of Hepatology, 62, S483-S484.
https://doi.org/10.1016/S0168-8278(15)30665-6

Volarevic V, Paunović VG, Marković ZM, Marković-Simović B, Misirkić-Marjanović M, Todorović-Marković B, Bojic S, Vucicevic L, Jovanović SP, Arsenijević NN, Holclajtner-Antunović ID, Milosavljević M, Dramićanin M, Kravić-Stevović TK, Ćirić D, Lukić ML, Trajković VS. Graphene Quantum Dots Attenuate Concanavalin A-Induced Hepatitis. in Journal of Hepatology. 2015;62:S483-S484.
doi:10.1016/S0168-8278(15)30665-6 .

Volarevic, V., Paunović, Verica G., Marković, Zoran M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Todorović-Marković, Biljana, Bojic, S., Vucicevic, L., Jovanović, Svetlana P., Arsenijević, Nebojša N., Holclajtner-Antunović, Ivanka D., Milosavljević, Momir, Dramićanin, Miroslav, Kravić-Stevović, Tamara K., Ćirić, Darko, Lukić, M. L., Trajković, Vladimir S., "Graphene Quantum Dots Attenuate Concanavalin A-Induced Hepatitis" in Journal of Hepatology, 62 (2015):S483-S484,
https://doi.org/10.1016/S0168-8278(15)30665-6 . .

TY  - JOUR
AU  - Ristić, Biljana Z.
AU  - Milenković, Marina
AU  - Dakic, Ivana R.
AU  - Todorović-Marković, Biljana
AU  - Milosavljević, Momir
AU  - Budimir, Milica
AU  - Paunović, Verica G.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5964
AB  - Synthesis of new antibacterial agents is becoming increasingly important in light of the emerging antibiotic resistance. In the present study we report that electrochemically produced graphene quantum dots (GQD), a new class of carbon nanoparticles, generate reactive oxygen species when photoexcited (470 nm, 1 W), and kill two strains of pathogenic bacteria, methicillin-resistant Staphylococcus aureus and Escherichia coli. Bacterial killing was demonstrated by the reduction in number of bacterial colonies in a standard plate count method, the increase in propidium iodide uptake confirming the cell membrane damage, as well as by morphological defects visualized by atomic force microscopy. The induction of oxidative stress in bacteria exposed to photoexcited GQD was confirmed by staining with a redox-sensitive fluorochrome dihydrorhodamine 123. Neither GQD nor light exposure alone were able to cause oxidative stress and reduce the viability of bacteria. Importantly, mouse spleen cells were markedly less sensitive in the same experimental conditions, thus indicating a fairly selective antibacterial photodynamic action of GQD. (C) 2014 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - Photodynamic antibacterial effect of graphene quantum dots
VL  - 35
IS  - 15
SP  - 4428
EP  - 4435
DO  - 10.1016/j.biomaterials.2014.02.014
ER  - 

@article{
author = "Ristić, Biljana Z. and Milenković, Marina and Dakic, Ivana R. and Todorović-Marković, Biljana and Milosavljević, Momir and Budimir, Milica and Paunović, Verica G. and Dramićanin, Miroslav and Marković, Zoran M. and Trajković, Vladimir S.",
year = "2014",
abstract = "Synthesis of new antibacterial agents is becoming increasingly important in light of the emerging antibiotic resistance. In the present study we report that electrochemically produced graphene quantum dots (GQD), a new class of carbon nanoparticles, generate reactive oxygen species when photoexcited (470 nm, 1 W), and kill two strains of pathogenic bacteria, methicillin-resistant Staphylococcus aureus and Escherichia coli. Bacterial killing was demonstrated by the reduction in number of bacterial colonies in a standard plate count method, the increase in propidium iodide uptake confirming the cell membrane damage, as well as by morphological defects visualized by atomic force microscopy. The induction of oxidative stress in bacteria exposed to photoexcited GQD was confirmed by staining with a redox-sensitive fluorochrome dihydrorhodamine 123. Neither GQD nor light exposure alone were able to cause oxidative stress and reduce the viability of bacteria. Importantly, mouse spleen cells were markedly less sensitive in the same experimental conditions, thus indicating a fairly selective antibacterial photodynamic action of GQD. (C) 2014 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "Photodynamic antibacterial effect of graphene quantum dots",
volume = "35",
number = "15",
pages = "4428-4435",
doi = "10.1016/j.biomaterials.2014.02.014"
}

Ristić, B. Z., Milenković, M., Dakic, I. R., Todorović-Marković, B., Milosavljević, M., Budimir, M., Paunović, V. G., Dramićanin, M., Marković, Z. M.,& Trajković, V. S.. (2014). Photodynamic antibacterial effect of graphene quantum dots. in Biomaterials, 35(15), 4428-4435.
https://doi.org/10.1016/j.biomaterials.2014.02.014

Ristić BZ, Milenković M, Dakic IR, Todorović-Marković B, Milosavljević M, Budimir M, Paunović VG, Dramićanin M, Marković ZM, Trajković VS. Photodynamic antibacterial effect of graphene quantum dots. in Biomaterials. 2014;35(15):4428-4435.
doi:10.1016/j.biomaterials.2014.02.014 .

Ristić, Biljana Z., Milenković, Marina, Dakic, Ivana R., Todorović-Marković, Biljana, Milosavljević, Momir, Budimir, Milica, Paunović, Verica G., Dramićanin, Miroslav, Marković, Zoran M., Trajković, Vladimir S., "Photodynamic antibacterial effect of graphene quantum dots" in Biomaterials, 35, no. 15 (2014):4428-4435,
https://doi.org/10.1016/j.biomaterials.2014.02.014 . .

TY  - JOUR
AU  - Volarevic, Vladislav
AU  - Paunović, Verica G.
AU  - Marković, Zoran M.
AU  - Marković-Simović, Bojana
AU  - Misirkić-Marjanović, Maja
AU  - Todorović-Marković, Biljana
AU  - Bojic, Sanja
AU  - Vucicevic, Ljubica
AU  - Jovanović, Svetlana P.
AU  - Arsenijević, Nebojša N.
AU  - Holclajtner-Antunović, Ivanka D.
AU  - Milosavljević, Momir
AU  - Dramićanin, Miroslav
AU  - Kravić-Stevović, Tamara K.
AU  - Ćirić, Darko
AU  - Lukić, Miodrag L.
AU  - Trajković, Vladimir S.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/324
AB  - We investigated the effect of large (40 nm) graphene quantum dots (GQDs) in concanavalin A (Con A; 12 mg/kg i.v.)-induced mouse hepatitis, a T cell-mediated liver injury resembling fulminant hepatitis in humans. Intravenously injected GQDs (50 mg/kg) accumulated in liver and reduced Con A-mediated liver damage, as demonstrated by histopathological analysis and a decrease in liver lipid peroxidation and serum levels of liver transaminases. The cleavage of apoptotic markers caspase-3/PARP and mRNA levels of proapoptotic mediators Puma, Noxa, Bax, Bak1, Bim, Apaf1, and p21, as well as LC3-I conversion to autophagosome-associated LC3-II and expression of autophagy-related (Atg) genes Atg4b, Atg7, Atg12, and beclin-1, were attenuated by GQDs, indicating a decrease in both apoptosis and autophagy in the liver tissue. This was associated with the reduced liver infiltration of immune cells, particularly the T cells producing proinflammatory cytokine IFN-?, and a decrease in IFN-gamma serum levels. In the spleen of GQD-exposed mice, mRNA expression of IFN-? and its transcription factor T-bet was reduced, while that of the IL-33 ligand ST2 was increased. The hepatoprotective effect of GQDs was less pronounced in ST2-deficient mice, indicating that it might depend on ST2 upregulation. In vitro, GQDs inhibited splenocyte IFN-gamma production, reduced the activation of extracellular signal-regulated kinase in macrophage and T cell lines, inhibited macrophage production of the free radical nitric oxide, and reduced its cytotoxicity toward hepatocyte cell line HepG2. Therefore, GQDs alleviate immune-mediated fulminant hepatitis by interfering with T cell and macrophage activation and possibly by exerting a direct hepatoprotective effect.
T2  - ACS Nano
T1  - Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage
VL  - 8
IS  - 12
SP  - 12098
EP  - 12109
DO  - 10.1021/nn502466z
ER  - 

@article{
author = "Volarevic, Vladislav and Paunović, Verica G. and Marković, Zoran M. and Marković-Simović, Bojana and Misirkić-Marjanović, Maja and Todorović-Marković, Biljana and Bojic, Sanja and Vucicevic, Ljubica and Jovanović, Svetlana P. and Arsenijević, Nebojša N. and Holclajtner-Antunović, Ivanka D. and Milosavljević, Momir and Dramićanin, Miroslav and Kravić-Stevović, Tamara K. and Ćirić, Darko and Lukić, Miodrag L. and Trajković, Vladimir S.",
year = "2014",
abstract = "We investigated the effect of large (40 nm) graphene quantum dots (GQDs) in concanavalin A (Con A; 12 mg/kg i.v.)-induced mouse hepatitis, a T cell-mediated liver injury resembling fulminant hepatitis in humans. Intravenously injected GQDs (50 mg/kg) accumulated in liver and reduced Con A-mediated liver damage, as demonstrated by histopathological analysis and a decrease in liver lipid peroxidation and serum levels of liver transaminases. The cleavage of apoptotic markers caspase-3/PARP and mRNA levels of proapoptotic mediators Puma, Noxa, Bax, Bak1, Bim, Apaf1, and p21, as well as LC3-I conversion to autophagosome-associated LC3-II and expression of autophagy-related (Atg) genes Atg4b, Atg7, Atg12, and beclin-1, were attenuated by GQDs, indicating a decrease in both apoptosis and autophagy in the liver tissue. This was associated with the reduced liver infiltration of immune cells, particularly the T cells producing proinflammatory cytokine IFN-?, and a decrease in IFN-gamma serum levels. In the spleen of GQD-exposed mice, mRNA expression of IFN-? and its transcription factor T-bet was reduced, while that of the IL-33 ligand ST2 was increased. The hepatoprotective effect of GQDs was less pronounced in ST2-deficient mice, indicating that it might depend on ST2 upregulation. In vitro, GQDs inhibited splenocyte IFN-gamma production, reduced the activation of extracellular signal-regulated kinase in macrophage and T cell lines, inhibited macrophage production of the free radical nitric oxide, and reduced its cytotoxicity toward hepatocyte cell line HepG2. Therefore, GQDs alleviate immune-mediated fulminant hepatitis by interfering with T cell and macrophage activation and possibly by exerting a direct hepatoprotective effect.",
journal = "ACS Nano",
title = "Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage",
volume = "8",
number = "12",
pages = "12098-12109",
doi = "10.1021/nn502466z"
}

Volarevic, V., Paunović, V. G., Marković, Z. M., Marković-Simović, B., Misirkić-Marjanović, M., Todorović-Marković, B., Bojic, S., Vucicevic, L., Jovanović, S. P., Arsenijević, N. N., Holclajtner-Antunović, I. D., Milosavljević, M., Dramićanin, M., Kravić-Stevović, T. K., Ćirić, D., Lukić, M. L.,& Trajković, V. S.. (2014). Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage. in ACS Nano, 8(12), 12098-12109.
https://doi.org/10.1021/nn502466z

Volarevic V, Paunović VG, Marković ZM, Marković-Simović B, Misirkić-Marjanović M, Todorović-Marković B, Bojic S, Vucicevic L, Jovanović SP, Arsenijević NN, Holclajtner-Antunović ID, Milosavljević M, Dramićanin M, Kravić-Stevović TK, Ćirić D, Lukić ML, Trajković VS. Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage. in ACS Nano. 2014;8(12):12098-12109.
doi:10.1021/nn502466z .

Volarevic, Vladislav, Paunović, Verica G., Marković, Zoran M., Marković-Simović, Bojana, Misirkić-Marjanović, Maja, Todorović-Marković, Biljana, Bojic, Sanja, Vucicevic, Ljubica, Jovanović, Svetlana P., Arsenijević, Nebojša N., Holclajtner-Antunović, Ivanka D., Milosavljević, Momir, Dramićanin, Miroslav, Kravić-Stevović, Tamara K., Ćirić, Darko, Lukić, Miodrag L., Trajković, Vladimir S., "Large Graphene Quantum Dots Alleviate Immune-Mediated Liver Damage" in ACS Nano, 8, no. 12 (2014):12098-12109,
https://doi.org/10.1021/nn502466z . .

TY  - JOUR
AU  - Jokanović, Vukoman R.
AU  - Čolović, Božana M.
AU  - Jokanovic, B.
AU  - Rudolf, R.
AU  - Trajković, Vladimir S.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5956
AB  - The SiO2 thin films (STFs) were deposited on the surfaces of stainless steel tapes and their activity was particularly investigated from the aspect of the number density of hydroxyl groups on their surfaces. The calculation procedure of density of active OH groups includes determination of average length of silica chains that constitute silica sol particles with almost uniform size, on the base of thermogravimetric analysis. The size of SiO2 particles is analyzed by transmission electron microscopy and dynamic light scattering method. Fibroblast (L929) cell densities on the surfaces of these films were investigated using phase contrast microcopy. It was shown that there is a relationship between OH group densities and density of attached cells. Besides, the cytotoxicity effect was studied and compared for various thermally treated STFs. (c) 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 1707-1714, 2014.
T2  - Journal of Biomedical Materials Research. Part A
T1  - Relationship between activity of silica thin films and density of cells occupation
VL  - 102
IS  - 6
SP  - 1707
EP  - 1714
DO  - 10.1002/jbm.a.34844
ER  - 

@article{
author = "Jokanović, Vukoman R. and Čolović, Božana M. and Jokanovic, B. and Rudolf, R. and Trajković, Vladimir S.",
year = "2014",
abstract = "The SiO2 thin films (STFs) were deposited on the surfaces of stainless steel tapes and their activity was particularly investigated from the aspect of the number density of hydroxyl groups on their surfaces. The calculation procedure of density of active OH groups includes determination of average length of silica chains that constitute silica sol particles with almost uniform size, on the base of thermogravimetric analysis. The size of SiO2 particles is analyzed by transmission electron microscopy and dynamic light scattering method. Fibroblast (L929) cell densities on the surfaces of these films were investigated using phase contrast microcopy. It was shown that there is a relationship between OH group densities and density of attached cells. Besides, the cytotoxicity effect was studied and compared for various thermally treated STFs. (c) 2013 Wiley Periodicals, Inc. J Biomed Mater Res Part A: 102A: 1707-1714, 2014.",
journal = "Journal of Biomedical Materials Research. Part A",
title = "Relationship between activity of silica thin films and density of cells occupation",
volume = "102",
number = "6",
pages = "1707-1714",
doi = "10.1002/jbm.a.34844"
}

Jokanović, V. R., Čolović, B. M., Jokanovic, B., Rudolf, R.,& Trajković, V. S.. (2014). Relationship between activity of silica thin films and density of cells occupation. in Journal of Biomedical Materials Research. Part A, 102(6), 1707-1714.
https://doi.org/10.1002/jbm.a.34844

Jokanović VR, Čolović BM, Jokanovic B, Rudolf R, Trajković VS. Relationship between activity of silica thin films and density of cells occupation. in Journal of Biomedical Materials Research. Part A. 2014;102(6):1707-1714.
doi:10.1002/jbm.a.34844 .

Jokanović, Vukoman R., Čolović, Božana M., Jokanovic, B., Rudolf, R., Trajković, Vladimir S., "Relationship between activity of silica thin films and density of cells occupation" in Journal of Biomedical Materials Research. Part A, 102, no. 6 (2014):1707-1714,
https://doi.org/10.1002/jbm.a.34844 . .

TY  - JOUR
AU  - Jokanović, Vukoman R.
AU  - Čolović, Božana M.
AU  - Sikirić, Dutour M.
AU  - Trajković, Vladimir S.
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5166
AB  - Mesoporous silica materials have already proved to be non-toxic and biocompatible, and also to have large pore volume and very high specific surface area suitable for loading of small molecules. Having this in mind and the fact that silicon dioxide (SiO2) powders can be so designed to obtain particle structures organized at multi levels, SiO2 was chosen as a potential carrier for metronidazole, an antibiotic drug. SiO2 powder was synthesized in two stages: first silica sol was prepared by hydrothermal synthesis and second the sol was converted into powder by dry spraying with simultaneous incorporation of the antibiotic into its structure. Scanning and transmission electron microscopy study revealed very complex structure and sub-structure of SiO2 particles. Cell viability tests were used for estimation of cytotoxicity of so synthesized SiO2. The drug release data showed that the system can provide drug release for a long time. Also, the device behavior is fully predictable, according to our theoretical model of multilevel structure design, and gives many opportunities for model investigations of drug release and its kinetics. The pore sizes and their distribution were observed as a limiting factor of drug release kinetics. Therefore, as the pore sizes are given as a set of discrete values, the kinetics of drug release might also be given as a set of corresponding discrete values. (c) 2012 Elsevier B.V. All rights reserved.
T2  - Ultrasonics Sonochemistry
T1  - A new approach to the drug release kinetics of a discrete system: SiO2 system obtained by ultrasonic dry spraying
VL  - 20
IS  - 1
SP  - 535
EP  - 545
DO  - 10.1016/j.ultsonch.2012.08.015
ER  - 

@article{
author = "Jokanović, Vukoman R. and Čolović, Božana M. and Sikirić, Dutour M. and Trajković, Vladimir S.",
year = "2013",
abstract = "Mesoporous silica materials have already proved to be non-toxic and biocompatible, and also to have large pore volume and very high specific surface area suitable for loading of small molecules. Having this in mind and the fact that silicon dioxide (SiO2) powders can be so designed to obtain particle structures organized at multi levels, SiO2 was chosen as a potential carrier for metronidazole, an antibiotic drug. SiO2 powder was synthesized in two stages: first silica sol was prepared by hydrothermal synthesis and second the sol was converted into powder by dry spraying with simultaneous incorporation of the antibiotic into its structure. Scanning and transmission electron microscopy study revealed very complex structure and sub-structure of SiO2 particles. Cell viability tests were used for estimation of cytotoxicity of so synthesized SiO2. The drug release data showed that the system can provide drug release for a long time. Also, the device behavior is fully predictable, according to our theoretical model of multilevel structure design, and gives many opportunities for model investigations of drug release and its kinetics. The pore sizes and their distribution were observed as a limiting factor of drug release kinetics. Therefore, as the pore sizes are given as a set of discrete values, the kinetics of drug release might also be given as a set of corresponding discrete values. (c) 2012 Elsevier B.V. All rights reserved.",
journal = "Ultrasonics Sonochemistry",
title = "A new approach to the drug release kinetics of a discrete system: SiO2 system obtained by ultrasonic dry spraying",
volume = "20",
number = "1",
pages = "535-545",
doi = "10.1016/j.ultsonch.2012.08.015"
}

Jokanović, V. R., Čolović, B. M., Sikirić, D. M.,& Trajković, V. S.. (2013). A new approach to the drug release kinetics of a discrete system: SiO2 system obtained by ultrasonic dry spraying. in Ultrasonics Sonochemistry, 20(1), 535-545.
https://doi.org/10.1016/j.ultsonch.2012.08.015

Jokanović VR, Čolović BM, Sikirić DM, Trajković VS. A new approach to the drug release kinetics of a discrete system: SiO2 system obtained by ultrasonic dry spraying. in Ultrasonics Sonochemistry. 2013;20(1):535-545.
doi:10.1016/j.ultsonch.2012.08.015 .

Jokanović, Vukoman R., Čolović, Božana M., Sikirić, Dutour M., Trajković, Vladimir S., "A new approach to the drug release kinetics of a discrete system: SiO2 system obtained by ultrasonic dry spraying" in Ultrasonics Sonochemistry, 20, no. 1 (2013):535-545,
https://doi.org/10.1016/j.ultsonch.2012.08.015 . .

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Ristić, Biljana Z.
AU  - Arsikin, Katarina M.
AU  - Klisic, Djordje G.
AU  - Harhaji-Trajković, Ljubica M.
AU  - Todorović-Marković, Biljana
AU  - Kepić, Dejan P.
AU  - Kravić-Stevović, Tamara K.
AU  - Jovanović, Svetlana P.
AU  - Milenković, Marina
AU  - Milivojević, Dušan
AU  - Bumbaširević, Vladimir Ž.
AU  - Dramićanin, Miroslav
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5025
AB  - The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470 nm, 1 W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation. DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LOB protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity. (C) 2012 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - Graphene quantum dots as autophagy-inducing photodynamic agents
VL  - 33
IS  - 29
SP  - 7084
EP  - 7092
DO  - 10.1016/j.biomaterials.2012.06.060
ER  - 

@article{
author = "Marković, Zoran M. and Ristić, Biljana Z. and Arsikin, Katarina M. and Klisic, Djordje G. and Harhaji-Trajković, Ljubica M. and Todorović-Marković, Biljana and Kepić, Dejan P. and Kravić-Stevović, Tamara K. and Jovanović, Svetlana P. and Milenković, Marina and Milivojević, Dušan and Bumbaširević, Vladimir Ž. and Dramićanin, Miroslav and Trajković, Vladimir S.",
year = "2012",
abstract = "The excellent photoluminescent properties of graphene quantum dots (GQD) makes them suitable candidates for biomedical applications, but their cytotoxicity has not been extensively studied. Here we show that electrochemically produced GQD irradiated with blue light (470 nm, 1 W) generate reactive oxygen species, including singlet oxygen, and kill U251 human glioma cells by causing oxidative stress. The cell death induced by photoexcited GQD displayed morphological and/or biochemical characteristics of both apoptosis (phosphatidylserine externalization, caspase activation. DNA fragmentation) and autophagy (formation of autophagic vesicles, LC3-I/LC3-II conversion, degradation of autophagic target p62). Moreover, a genetic inactivation of autophagy-essential LOB protein partly abrogated the photodynamic cytotoxicity of GQD. These data indicate potential usefulness of GQD in photodynamic therapy, but also raise concerns about their possible toxicity. (C) 2012 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "Graphene quantum dots as autophagy-inducing photodynamic agents",
volume = "33",
number = "29",
pages = "7084-7092",
doi = "10.1016/j.biomaterials.2012.06.060"
}

Marković, Z. M., Ristić, B. Z., Arsikin, K. M., Klisic, D. G., Harhaji-Trajković, L. M., Todorović-Marković, B., Kepić, D. P., Kravić-Stevović, T. K., Jovanović, S. P., Milenković, M., Milivojević, D., Bumbaširević, V. Ž., Dramićanin, M.,& Trajković, V. S.. (2012). Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials, 33(29), 7084-7092.
https://doi.org/10.1016/j.biomaterials.2012.06.060

Marković ZM, Ristić BZ, Arsikin KM, Klisic DG, Harhaji-Trajković LM, Todorović-Marković B, Kepić DP, Kravić-Stevović TK, Jovanović SP, Milenković M, Milivojević D, Bumbaširević VŽ, Dramićanin M, Trajković VS. Graphene quantum dots as autophagy-inducing photodynamic agents. in Biomaterials. 2012;33(29):7084-7092.
doi:10.1016/j.biomaterials.2012.06.060 .

Marković, Zoran M., Ristić, Biljana Z., Arsikin, Katarina M., Klisic, Djordje G., Harhaji-Trajković, Ljubica M., Todorović-Marković, Biljana, Kepić, Dejan P., Kravić-Stevović, Tamara K., Jovanović, Svetlana P., Milenković, Marina, Milivojević, Dušan, Bumbaširević, Vladimir Ž., Dramićanin, Miroslav, Trajković, Vladimir S., "Graphene quantum dots as autophagy-inducing photodynamic agents" in Biomaterials, 33, no. 29 (2012):7084-7092,
https://doi.org/10.1016/j.biomaterials.2012.06.060 . .

TY  - JOUR
AU  - Stevanović, Darko
AU  - Starčević, Vesna
AU  - Vilimanovich, Urosh
AU  - Nešić, Dejan
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Savić, Emina
AU  - Popadic, Dusan
AU  - Sudar, Emina
AU  - Micic, Dragan
AU  - Šumarac-Dumanović, Mirjana
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4590
AB  - We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.
T2  - Brain Behavior and Immunity
T1  - Immunomodulatory actions of central ghrelin in diet-induced energy imbalance
VL  - 26
IS  - 1
SP  - 150
EP  - 158
DO  - 10.1016/j.bbi.2011.08.009
ER  - 

@article{
author = "Stevanović, Darko and Starčević, Vesna and Vilimanovich, Urosh and Nešić, Dejan and Vucicevic, Ljubica and Misirkić, Maja and Janjetović, Kristina D. and Savić, Emina and Popadic, Dusan and Sudar, Emina and Micic, Dragan and Šumarac-Dumanović, Mirjana and Trajković, Vladimir S.",
year = "2012",
abstract = "We investigated the effects of centrally administered orexigenic hormone ghrelin on energy imbalance-induced inflammation. Rats were subjected for four weeks to three different dietary regimes: normal (standard food), high-fat (standard food with 30% lard) or food-restricted (70%, 50%, 40% and 40% of the expected food intake in 1st, 2nd, 3rd and 4th week, respectively). Compared to normal-weight controls, starved, but not obese rats had significantly higher levels of proinflammatory cytokines (TNF, IL-1 beta, IFN-gamma) in the blood. When compared to normally fed animals, the hearts of starved and obese animals expressed higher levels of mRNAs encoding proinflammatory mediators (TNF, IL-1 beta, IL-6, IFN-gamma, IL-17, IL-12, iNOS), while mRNA levels of the anti-inflammatory TGF-beta remained unchanged. Intracerebroventricular (ICV) injection of ghrelin (1 mu g/day) for five consecutive days significantly reduced TNF, IL-1 beta and IFN-gamma levels in the blood of starved rats, as well as TNF, IL-17 and IL-12p40 mRNA expression in the hearts of obese rats. Conversely, ICV ghrelin increased the levels of 1FN-gamma, IL-17,1L-12p35 and IL-12p40 mRNA in the heart tissue of food-restricted animals. This was associated with an increase of immunosuppressive ACTH/corticosterone production in starved animals and a decrease of the immunostimulatory adipokine leptin both in food-restricted and high-fat groups. Ghrelin activated the energy sensor AMP-activated protein kinase (AMPK) in the hypothalamus and inhibited extracellular signal-regulated kinase (ERK) in the hearts of obese, but not starved rats. Therefore, central ghrelin may play a complex role in energy imbalance-induced inflammation by modulating HPA axis, leptin and AMPK/ERK signaling pathways. (C) 2011 Elsevier Inc. All rights reserved.",
journal = "Brain Behavior and Immunity",
title = "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance",
volume = "26",
number = "1",
pages = "150-158",
doi = "10.1016/j.bbi.2011.08.009"
}

Stevanović, D., Starčević, V., Vilimanovich, U., Nešić, D., Vucicevic, L., Misirkić, M., Janjetović, K. D., Savić, E., Popadic, D., Sudar, E., Micic, D., Šumarac-Dumanović, M.,& Trajković, V. S.. (2012). Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity, 26(1), 150-158.
https://doi.org/10.1016/j.bbi.2011.08.009

Stevanović D, Starčević V, Vilimanovich U, Nešić D, Vucicevic L, Misirkić M, Janjetović KD, Savić E, Popadic D, Sudar E, Micic D, Šumarac-Dumanović M, Trajković VS. Immunomodulatory actions of central ghrelin in diet-induced energy imbalance. in Brain Behavior and Immunity. 2012;26(1):150-158.
doi:10.1016/j.bbi.2011.08.009 .

Stevanović, Darko, Starčević, Vesna, Vilimanovich, Urosh, Nešić, Dejan, Vucicevic, Ljubica, Misirkić, Maja, Janjetović, Kristina D., Savić, Emina, Popadic, Dusan, Sudar, Emina, Micic, Dragan, Šumarac-Dumanović, Mirjana, Trajković, Vladimir S., "Immunomodulatory actions of central ghrelin in diet-induced energy imbalance" in Brain Behavior and Immunity, 26, no. 1 (2012):150-158,
https://doi.org/10.1016/j.bbi.2011.08.009 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5156
AB  - The fullerene C-60, due to the physicochemical properties of its spherical cage-like molecule build exclusively from carbon atoms, is able to both scavenge and generate reactive oxygen species. While this unique dual property could be exploited in biomedicine, the low water solubility of C-60 hampers the investigation of its behavior in biological systems. The C-60 can be brought into water by solvent extraction, by complexation with surfactants/polymers, or by long-term stirring, yielding pristine (unmodified) fullerene suspensions. On the other hand, a modification of the C-60 core by the attachment of various functional groups results in the formation of water-soluble fullerene derivatives. Assessment of toxicity associated with C-60 preparations is of pivotal importance for their biomedical application as cytoprotective (antioxidant), cytotoxic (anticancer), or drug delivery agents. Moreover, the widespread industrial utilization of fullerenes may also have implications for human health. However, the alterations in physicochemical properties imposed by the utilization of different methods for C-60 solubilization profoundly influence toxicological effects of fullerene preparations, thus making the analysis of their potential therapeutic and environmental toxicity difficult. This review provides a comprehensive evaluation of the in vitro and in vivo toxicity of fullerenes, focusing on the comparison between pristine and derivatized C-60 preparations and the mechanisms of their toxicity to mammalian cells and tissues.
T2  - Archives of Toxicology
T1  - Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress
VL  - 86
IS  - 12
SP  - 1809
EP  - 1827
DO  - 10.1007/s00204-012-0859-6
ER  - 

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Trajković, Vladimir S.",
year = "2012",
abstract = "The fullerene C-60, due to the physicochemical properties of its spherical cage-like molecule build exclusively from carbon atoms, is able to both scavenge and generate reactive oxygen species. While this unique dual property could be exploited in biomedicine, the low water solubility of C-60 hampers the investigation of its behavior in biological systems. The C-60 can be brought into water by solvent extraction, by complexation with surfactants/polymers, or by long-term stirring, yielding pristine (unmodified) fullerene suspensions. On the other hand, a modification of the C-60 core by the attachment of various functional groups results in the formation of water-soluble fullerene derivatives. Assessment of toxicity associated with C-60 preparations is of pivotal importance for their biomedical application as cytoprotective (antioxidant), cytotoxic (anticancer), or drug delivery agents. Moreover, the widespread industrial utilization of fullerenes may also have implications for human health. However, the alterations in physicochemical properties imposed by the utilization of different methods for C-60 solubilization profoundly influence toxicological effects of fullerene preparations, thus making the analysis of their potential therapeutic and environmental toxicity difficult. This review provides a comprehensive evaluation of the in vitro and in vivo toxicity of fullerenes, focusing on the comparison between pristine and derivatized C-60 preparations and the mechanisms of their toxicity to mammalian cells and tissues.",
journal = "Archives of Toxicology",
title = "Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress",
volume = "86",
number = "12",
pages = "1809-1827",
doi = "10.1007/s00204-012-0859-6"
}

Trpković, A., Todorović-Marković, B.,& Trajković, V. S.. (2012). Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress. in Archives of Toxicology, 86(12), 1809-1827.
https://doi.org/10.1007/s00204-012-0859-6

Trpković A, Todorović-Marković B, Trajković VS. Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress. in Archives of Toxicology. 2012;86(12):1809-1827.
doi:10.1007/s00204-012-0859-6 .

Trpković, Andreja, Todorović-Marković, Biljana, Trajković, Vladimir S., "Toxicity of pristine versus functionalized fullerenes: mechanisms of cell damage and the role of oxidative stress" in Archives of Toxicology, 86, no. 12 (2012):1809-1827,
https://doi.org/10.1007/s00204-012-0859-6 . .

TY  - JOUR
AU  - Klionsky, Daniel J.
AU  - Trajković, Vladimir S.
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4894
AB  - In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.
T2  - Autophagy
T1  - Guidelines for the use and interpretation of assays for monitoring autophagy
VL  - 8
IS  - 4
SP  - 445
EP  - 544
DO  - 10.4161/auto.19496
ER  - 

@article{
author = "Klionsky, Daniel J. and Trajković, Vladimir S.",
year = "2012",
abstract = "In 2008 we published the first set of guidelines for standardizing research in autophagy. Since then, research on this topic has continued to accelerate, and many new scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Accordingly, it is important to update these guidelines for monitoring autophagy in different organisms. Various reviews have described the range of assays that have been used for this purpose. Nevertheless, there continues to be confusion regarding acceptable methods to measure autophagy, especially in multicellular eukaryotes. A key point that needs to be emphasized is that there is a difference between measurements that monitor the numbers or volume of autophagic elements (e.g., autophagosomes or autolysosomes) at any stage of the autophagic process vs. those that measure flux through the autophagy pathway (i.e., the complete process); thus, a block in macroautophagy that results in autophagosome accumulation needs to be differentiated from stimuli that result in increased autophagic activity, defined as increased autophagy induction coupled with increased delivery to, and degradation within, lysosomes (in most higher eukaryotes and some protists such as Dictyostelium) or the vacuole (in plants and fungi). In other words, it is especially important that investigators new to the field understand that the appearance of more autophagosomes does not necessarily equate with more autophagy. In fact, in many cases, autophagosomes accumulate because of a block in trafficking to lysosomes without a concomitant change in autophagosome biogenesis, whereas an increase in autolysosomes may reflect a reduction in degradative activity. Here, we present a set of guidelines for the selection and interpretation of methods for use by investigators who aim to examine macroautophagy and related processes, as well as for reviewers who need to provide realistic and reasonable critiques of papers that are focused on these processes. These guidelines are not meant to be a formulaic set of rules, because the appropriate assays depend in part on the question being asked and the system being used. In addition, we emphasize that no individual assay is guaranteed to be the most appropriate one in every situation, and we strongly recommend the use of multiple assays to monitor autophagy. In these guidelines, we consider these various methods of assessing autophagy and what information can, or cannot, be obtained from them. Finally, by discussing the merits and limits of particular autophagy assays, we hope to encourage technical innovation in the field.",
journal = "Autophagy",
title = "Guidelines for the use and interpretation of assays for monitoring autophagy",
volume = "8",
number = "4",
pages = "445-544",
doi = "10.4161/auto.19496"
}

Klionsky, D. J.,& Trajković, V. S.. (2012). Guidelines for the use and interpretation of assays for monitoring autophagy. in Autophagy, 8(4), 445-544.
https://doi.org/10.4161/auto.19496

Klionsky DJ, Trajković VS. Guidelines for the use and interpretation of assays for monitoring autophagy. in Autophagy. 2012;8(4):445-544.
doi:10.4161/auto.19496 .

Klionsky, Daniel J., Trajković, Vladimir S., "Guidelines for the use and interpretation of assays for monitoring autophagy" in Autophagy, 8, no. 4 (2012):445-544,
https://doi.org/10.4161/auto.19496 . .

TY  - JOUR
AU  - Marković, Zoran M.
AU  - Harhaji-Trajković, Ljubica M.
AU  - Todorović-Marković, Biljana
AU  - Kepić, Dejan P.
AU  - Arsikin, Katarina M.
AU  - Jovanović, Svetlana P.
AU  - Pantovic, Aleksandar C.
AU  - Dramićanin, Miroslav
AU  - Trajković, Vladimir S.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4179
AB  - The present study compared the photothermal anticancer activity of near-infrared (NIR)-excited graphene nanoparticles and carbon nanotubes (CNT). Despite lower NIR-absorbing capacity, suspension of polyvinylpyrrolidone-coated graphene sheets exposed to NIR radiation (808 nm, 2 W/cm(2)) generated more heat than DNA or sodium dodecylbenzenesulfonate-solubilized single-wall CNT under the same conditions. Accordingly, graphene nanoparticles performed significantly better than CNT in inducing photothermal death of U251 human glioma cells in vitro. The superior photothermal sensitivity of graphene sheets could be largely explained by their better dispersivity, which has been supported by a simple calculation taking into account thermodynamic, optical and geometrical properties of the two type of carbon nanoparticles. The mechanisms of graphene-mediated photothermal killing of cancer cells apparently involved oxidative stress and mitochondrial membrane depolarization resulting in mixed apoptotic and necrotic cell death characterized by caspase activation/DNA fragmentation and cell membrane damage, respectively. (c) 2010 Elsevier Ltd. All rights reserved.
T2  - Biomaterials
T1  - In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes
VL  - 32
IS  - 4
SP  - 1121
EP  - 1129
DO  - 10.1016/j.biomaterials.2010.10.030
ER  - 

@article{
author = "Marković, Zoran M. and Harhaji-Trajković, Ljubica M. and Todorović-Marković, Biljana and Kepić, Dejan P. and Arsikin, Katarina M. and Jovanović, Svetlana P. and Pantovic, Aleksandar C. and Dramićanin, Miroslav and Trajković, Vladimir S.",
year = "2011",
abstract = "The present study compared the photothermal anticancer activity of near-infrared (NIR)-excited graphene nanoparticles and carbon nanotubes (CNT). Despite lower NIR-absorbing capacity, suspension of polyvinylpyrrolidone-coated graphene sheets exposed to NIR radiation (808 nm, 2 W/cm(2)) generated more heat than DNA or sodium dodecylbenzenesulfonate-solubilized single-wall CNT under the same conditions. Accordingly, graphene nanoparticles performed significantly better than CNT in inducing photothermal death of U251 human glioma cells in vitro. The superior photothermal sensitivity of graphene sheets could be largely explained by their better dispersivity, which has been supported by a simple calculation taking into account thermodynamic, optical and geometrical properties of the two type of carbon nanoparticles. The mechanisms of graphene-mediated photothermal killing of cancer cells apparently involved oxidative stress and mitochondrial membrane depolarization resulting in mixed apoptotic and necrotic cell death characterized by caspase activation/DNA fragmentation and cell membrane damage, respectively. (c) 2010 Elsevier Ltd. All rights reserved.",
journal = "Biomaterials",
title = "In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes",
volume = "32",
number = "4",
pages = "1121-1129",
doi = "10.1016/j.biomaterials.2010.10.030"
}

Marković, Z. M., Harhaji-Trajković, L. M., Todorović-Marković, B., Kepić, D. P., Arsikin, K. M., Jovanović, S. P., Pantovic, A. C., Dramićanin, M.,& Trajković, V. S.. (2011). In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes. in Biomaterials, 32(4), 1121-1129.
https://doi.org/10.1016/j.biomaterials.2010.10.030

Marković ZM, Harhaji-Trajković LM, Todorović-Marković B, Kepić DP, Arsikin KM, Jovanović SP, Pantovic AC, Dramićanin M, Trajković VS. In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes. in Biomaterials. 2011;32(4):1121-1129.
doi:10.1016/j.biomaterials.2010.10.030 .

Marković, Zoran M., Harhaji-Trajković, Ljubica M., Todorović-Marković, Biljana, Kepić, Dejan P., Arsikin, Katarina M., Jovanović, Svetlana P., Pantovic, Aleksandar C., Dramićanin, Miroslav, Trajković, Vladimir S., "In vitro comparison of the photothermal anticancer activity of graphene nanoparticles and carbon nanotubes" in Biomaterials, 32, no. 4 (2011):1121-1129,
https://doi.org/10.1016/j.biomaterials.2010.10.030 . .

TY  - JOUR
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Vilimanovich, Urosh
AU  - Tovilovic, Gordana
AU  - Zogovic, Nevena
AU  - Nikolić, Zoran M.
AU  - Jovanović, Svetlana P.
AU  - Bumbaširević, Vladimir Ž.
AU  - Trajković, Vladimir S.
AU  - Harhaji-Trajković, Ljubica M.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4205
AB  - Metformin is an antidiabetic drug with anticancer properties, which mainly acts through induction of AMP-activated protein kinase (AMPK). In the present study we investigated the influence of metformin on the in vitro anticancer activity of the well-known chemotherapeutic agent cisplatin. Cell viability was determined by MTT and LDH release assay, oxidative stress and apoptosis (caspase activation, DNA fragmentation, and phosphatidylserine exposure) were assessed by flow cytometry, while activation of AMPK and Akt was analyzed by immunoblotting. Although metformin reduced the number of tumour cells when applied alone, it surprisingly antagonized the cytotoxicity of cisplatin towards U251 human glioma, C6 rat glioma, SHSY5Y human neuroblastoma, L929 mouse fibrosarcoma and HL-60 human leukemia cell lines. Only in B16 mouse melanoma cells metformin augmented the cytotoxicity of cisplatin. In U251 glioma cells metformin suppressed cisplatin-induced apoptotic cell death through inhibition of oxidative stress and caspase activation. The observed cytoprotection was apparently AMPK-independent, as metformin did not further increase cisplatin-induced AMPK activation in U251 cells and other pharmacological AMPK activators failed to block cisplatin-mediated apoptosis. On the other hand, metformin induced Akt activation in cisplatin-treated cells and Akt inhibitor 10-DEBC hydrochloride or phosphoinositide 3-kinase/Akt inhibitor LY294002 abolished metformin-mediated antioxidant and antiapoptotic effects. In conclusion, the antidiabetic drug metformin reduces cisplatin in vitro anticancer activity through AMPK-independent upregulation of Akt survival pathway. These data warrant caution when considering metformin for treatment of diabetic cancer patients receiving cisplatin or as a potential adjuvant in cisplatin-based chemotherapeutic regimens. (c) 2010 Published by Elsevier B.V.
T2  - European Journal of Pharmacology
T1  - Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt
VL  - 651
IS  - 1-3
SP  - 41
EP  - 50
DO  - 10.1016/j.ejphar.2010.11.005
ER  - 

@article{
author = "Janjetović, Kristina D. and Vucicevic, Ljubica and Misirkić, Maja and Vilimanovich, Urosh and Tovilovic, Gordana and Zogovic, Nevena and Nikolić, Zoran M. and Jovanović, Svetlana P. and Bumbaširević, Vladimir Ž. and Trajković, Vladimir S. and Harhaji-Trajković, Ljubica M.",
year = "2011",
abstract = "Metformin is an antidiabetic drug with anticancer properties, which mainly acts through induction of AMP-activated protein kinase (AMPK). In the present study we investigated the influence of metformin on the in vitro anticancer activity of the well-known chemotherapeutic agent cisplatin. Cell viability was determined by MTT and LDH release assay, oxidative stress and apoptosis (caspase activation, DNA fragmentation, and phosphatidylserine exposure) were assessed by flow cytometry, while activation of AMPK and Akt was analyzed by immunoblotting. Although metformin reduced the number of tumour cells when applied alone, it surprisingly antagonized the cytotoxicity of cisplatin towards U251 human glioma, C6 rat glioma, SHSY5Y human neuroblastoma, L929 mouse fibrosarcoma and HL-60 human leukemia cell lines. Only in B16 mouse melanoma cells metformin augmented the cytotoxicity of cisplatin. In U251 glioma cells metformin suppressed cisplatin-induced apoptotic cell death through inhibition of oxidative stress and caspase activation. The observed cytoprotection was apparently AMPK-independent, as metformin did not further increase cisplatin-induced AMPK activation in U251 cells and other pharmacological AMPK activators failed to block cisplatin-mediated apoptosis. On the other hand, metformin induced Akt activation in cisplatin-treated cells and Akt inhibitor 10-DEBC hydrochloride or phosphoinositide 3-kinase/Akt inhibitor LY294002 abolished metformin-mediated antioxidant and antiapoptotic effects. In conclusion, the antidiabetic drug metformin reduces cisplatin in vitro anticancer activity through AMPK-independent upregulation of Akt survival pathway. These data warrant caution when considering metformin for treatment of diabetic cancer patients receiving cisplatin or as a potential adjuvant in cisplatin-based chemotherapeutic regimens. (c) 2010 Published by Elsevier B.V.",
journal = "European Journal of Pharmacology",
title = "Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt",
volume = "651",
number = "1-3",
pages = "41-50",
doi = "10.1016/j.ejphar.2010.11.005"
}

Janjetović, K. D., Vucicevic, L., Misirkić, M., Vilimanovich, U., Tovilovic, G., Zogovic, N., Nikolić, Z. M., Jovanović, S. P., Bumbaširević, V. Ž., Trajković, V. S.,& Harhaji-Trajković, L. M.. (2011). Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt. in European Journal of Pharmacology, 651(1-3), 41-50.
https://doi.org/10.1016/j.ejphar.2010.11.005

Janjetović KD, Vucicevic L, Misirkić M, Vilimanovich U, Tovilovic G, Zogovic N, Nikolić ZM, Jovanović SP, Bumbaširević VŽ, Trajković VS, Harhaji-Trajković LM. Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt. in European Journal of Pharmacology. 2011;651(1-3):41-50.
doi:10.1016/j.ejphar.2010.11.005 .

Janjetović, Kristina D., Vucicevic, Ljubica, Misirkić, Maja, Vilimanovich, Urosh, Tovilovic, Gordana, Zogovic, Nevena, Nikolić, Zoran M., Jovanović, Svetlana P., Bumbaširević, Vladimir Ž., Trajković, Vladimir S., Harhaji-Trajković, Ljubica M., "Metformin reduces cisplatin-mediated apoptotic death of cancer cells through AMPK-independent activation of Akt" in European Journal of Pharmacology, 651, no. 1-3 (2011):41-50,
https://doi.org/10.1016/j.ejphar.2010.11.005 . .

TY  - JOUR
AU  - Sudar, Emina
AU  - Dobutović, Branislava
AU  - Soskić, Sanja S.
AU  - Mandušić, Vesna
AU  - Žakula, Zorica
AU  - Misirkić, Maja
AU  - Vucicevic, Ljubica
AU  - Janjetović, Kristina D.
AU  - Trajković, Vladimir S.
AU  - Mikhailidis, Dimitri P.
AU  - Isenović, Esma R.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4317
AB  - The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.
T2  - Journal of Physiology and Biochemistry
T1  - Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats
VL  - 67
IS  - 2
SP  - 195
EP  - 204
DO  - 10.1007/s13105-010-0063-1
ER  - 

@article{
author = "Sudar, Emina and Dobutović, Branislava and Soskić, Sanja S. and Mandušić, Vesna and Žakula, Zorica and Misirkić, Maja and Vucicevic, Ljubica and Janjetović, Kristina D. and Trajković, Vladimir S. and Mikhailidis, Dimitri P. and Isenović, Esma R.",
year = "2011",
abstract = "The purpose of this study was to examine the effects of ghrelin on protein kinase B (Akt) and mitogen-activated protein kinase p42/44 (ERK1/2) activation as well as ghrelin effects on inducible nitric oxide (NO) synthase (iNOS; for gene Nos2) activity/expression in rat hearts. Male Wistar rats were treated with ghrelin (0.3 nmol/5 mu l) or an equal volume of phosphate-buffered saline, injected every 24 h into the lateral cerebral ventricle for 5 days and 2 h after the last treatment the animals were sacrificed. Serum NO, l-arginine (l-Arg), and arginase activity were measured spectrophotometrically. For phosphorylation of Akt, ERK1/2, and iNOS protein expression, Western blot method was used. The expression of Nos2 mRNA was measured by the quantitative real-time polymerase chain reaction (qRT-PCR). Treatment with ghrelin significantly increased NO production in serum by 1.4-fold compared with control. The concentration of l-Arg was significantly higher in ghrelin-treated rats than in control while arginase activity was significantly lower in ghrelin-treated than in control hearts. Ghrelin treatment increased phosphorylation of Akt by 1.9-fold and ERK1/2 by 1.6-fold and increased iNOS expression by 2.5-fold compared with control. In addition, ghrelin treatment increased Nos2 gene expression by 2.2-fold as determined by qRT-PCR. These results indicate that ghrelin regulation of iNOS expression/activity is mediated via Akt/ERK1/2 signaling pathway. These results may be relevant to understanding molecular mechanisms underlying direct cardiovascular actions of ghrelin.",
journal = "Journal of Physiology and Biochemistry",
title = "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats",
volume = "67",
number = "2",
pages = "195-204",
doi = "10.1007/s13105-010-0063-1"
}

Sudar, E., Dobutović, B., Soskić, S. S., Mandušić, V., Žakula, Z., Misirkić, M., Vucicevic, L., Janjetović, K. D., Trajković, V. S., Mikhailidis, D. P.,& Isenović, E. R.. (2011). Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry, 67(2), 195-204.
https://doi.org/10.1007/s13105-010-0063-1

Sudar E, Dobutović B, Soskić SS, Mandušić V, Žakula Z, Misirkić M, Vucicevic L, Janjetović KD, Trajković VS, Mikhailidis DP, Isenović ER. Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats. in Journal of Physiology and Biochemistry. 2011;67(2):195-204.
doi:10.1007/s13105-010-0063-1 .

Sudar, Emina, Dobutović, Branislava, Soskić, Sanja S., Mandušić, Vesna, Žakula, Zorica, Misirkić, Maja, Vucicevic, Ljubica, Janjetović, Kristina D., Trajković, Vladimir S., Mikhailidis, Dimitri P., Isenović, Esma R., "Regulation of inducible nitric oxide synthase activity/expression in rat hearts from ghrelin-treated rats" in Journal of Physiology and Biochemistry, 67, no. 2 (2011):195-204,
https://doi.org/10.1007/s13105-010-0063-1 . .

TY  - JOUR
AU  - Vucicevic, Ljubica
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vilimanovich, Urosh
AU  - Sudar, Emina
AU  - Isenović, Esma R.
AU  - Prica, Marko
AU  - Harhaji-Trajković, Ljubica M.
AU  - Kravić-Stevović, Tamara K.
AU  - Bumbaširević, Vladimir Ž.
AU  - Trajković, Vladimir S.
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4180
AB  - In the present study, we report that compound C, an inhibitor of a key intracellular energy sensor AMP-activated protein kinase (AMPK), can induce autophagy in cancer cells. The induction of autophagy in U251 human glioma cell line was demonstrated by acridine orange staining of intracellular acidic vesicles, Beclin 1 induction, p62 decrease and conversion of LC3-I to autophagosome-associated LC3-II in the presence of proteolysis inhibitors. The presence of autophagosome-like vesicles was confirmed by transmission electron microscopy. Compound C-mediated inhibition of AMPK and raptor in U251 cells was associated with paradoxical decrease in phosphorylation of AMPK/raptor-repressed mTOR, a major negative regulator of autophagy, and its downstream target p70S6K. The phosphorylation of an mTOR activator Akt and the PI3K-activating kinase Src was also impaired in compound C-treated cells. The siRNA-mediated AMPK silencing did not reduce the activity of the Akt/mTOR/p70S6K pathway and AMPK activators metformin and AICAR failed to block compound C-induced autophagy. Autophagy inhibitors bafilomycin and chloroquine significantly increased the cytotoxicity of compound C towards U251 cells, as confirmed by increase in lactate dehydrogenase release, DNA fragmentation and caspase-3 activation. Similar effects of compound C were also observed in C6 rat glioma, L929 mouse fibrosarcoma and B16 mouse melanoma cell lines. Since compound C has previously been reported to suppress AMPK-dependent autophagy in different cell types, our findings suggest that the effects of compound C on autophagy might be dose-, cell type- and/or context-dependent. By demonstrating the ability of compound C to induce autophagic response in cancer cells via AMPK inhibition-independent downregulation of Akt/mTOR pathway, our results warrant caution when using compound C to inhibit AMPK-dependent cellular responses, but also support further exploration of compound C and related molecules as potential anticancer agents.
T2  - Autophagy
T1  - Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway
VL  - 7
IS  - 1
SP  - 40
EP  - 50
DO  - 10.4161/auto.7.1.13883
ER  - 

@article{
author = "Vucicevic, Ljubica and Misirkić, Maja and Janjetović, Kristina D. and Vilimanovich, Urosh and Sudar, Emina and Isenović, Esma R. and Prica, Marko and Harhaji-Trajković, Ljubica M. and Kravić-Stevović, Tamara K. and Bumbaširević, Vladimir Ž. and Trajković, Vladimir S.",
year = "2011",
abstract = "In the present study, we report that compound C, an inhibitor of a key intracellular energy sensor AMP-activated protein kinase (AMPK), can induce autophagy in cancer cells. The induction of autophagy in U251 human glioma cell line was demonstrated by acridine orange staining of intracellular acidic vesicles, Beclin 1 induction, p62 decrease and conversion of LC3-I to autophagosome-associated LC3-II in the presence of proteolysis inhibitors. The presence of autophagosome-like vesicles was confirmed by transmission electron microscopy. Compound C-mediated inhibition of AMPK and raptor in U251 cells was associated with paradoxical decrease in phosphorylation of AMPK/raptor-repressed mTOR, a major negative regulator of autophagy, and its downstream target p70S6K. The phosphorylation of an mTOR activator Akt and the PI3K-activating kinase Src was also impaired in compound C-treated cells. The siRNA-mediated AMPK silencing did not reduce the activity of the Akt/mTOR/p70S6K pathway and AMPK activators metformin and AICAR failed to block compound C-induced autophagy. Autophagy inhibitors bafilomycin and chloroquine significantly increased the cytotoxicity of compound C towards U251 cells, as confirmed by increase in lactate dehydrogenase release, DNA fragmentation and caspase-3 activation. Similar effects of compound C were also observed in C6 rat glioma, L929 mouse fibrosarcoma and B16 mouse melanoma cell lines. Since compound C has previously been reported to suppress AMPK-dependent autophagy in different cell types, our findings suggest that the effects of compound C on autophagy might be dose-, cell type- and/or context-dependent. By demonstrating the ability of compound C to induce autophagic response in cancer cells via AMPK inhibition-independent downregulation of Akt/mTOR pathway, our results warrant caution when using compound C to inhibit AMPK-dependent cellular responses, but also support further exploration of compound C and related molecules as potential anticancer agents.",
journal = "Autophagy",
title = "Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway",
volume = "7",
number = "1",
pages = "40-50",
doi = "10.4161/auto.7.1.13883"
}

Vucicevic, L., Misirkić, M., Janjetović, K. D., Vilimanovich, U., Sudar, E., Isenović, E. R., Prica, M., Harhaji-Trajković, L. M., Kravić-Stevović, T. K., Bumbaširević, V. Ž.,& Trajković, V. S.. (2011). Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway. in Autophagy, 7(1), 40-50.
https://doi.org/10.4161/auto.7.1.13883

Vucicevic L, Misirkić M, Janjetović KD, Vilimanovich U, Sudar E, Isenović ER, Prica M, Harhaji-Trajković LM, Kravić-Stevović TK, Bumbaširević VŽ, Trajković VS. Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway. in Autophagy. 2011;7(1):40-50.
doi:10.4161/auto.7.1.13883 .

Vucicevic, Ljubica, Misirkić, Maja, Janjetović, Kristina D., Vilimanovich, Urosh, Sudar, Emina, Isenović, Esma R., Prica, Marko, Harhaji-Trajković, Ljubica M., Kravić-Stevović, Tamara K., Bumbaširević, Vladimir Ž., Trajković, Vladimir S., "Compound C induces protective autophagy in cancer cells through AMPK inhibition-independent blockade of Akt/mTOR pathway" in Autophagy, 7, no. 1 (2011):40-50,
https://doi.org/10.4161/auto.7.1.13883 . .

TY  - JOUR
AU  - Trpković, Andreja
AU  - Todorović-Marković, Biljana
AU  - Kleut, Duška
AU  - Misirkić, Maja
AU  - Janjetović, Kristina D.
AU  - Vucicevic, Ljubica
AU  - Pantovic, Aleksandar
AU  - Jovanović, Svetlana P.
AU  - Dramićanin, Miroslav
AU  - Marković, Zoran M.
AU  - Trajković, Vladimir S.
PY  - 2010
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4093
AB  - The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.
T2  - Nanotechnology
T1  - Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles
VL  - 21
IS  - 37
DO  - 10.1088/0957-4484/21/37/375102
ER  - 

@article{
author = "Trpković, Andreja and Todorović-Marković, Biljana and Kleut, Duška and Misirkić, Maja and Janjetović, Kristina D. and Vucicevic, Ljubica and Pantovic, Aleksandar and Jovanović, Svetlana P. and Dramićanin, Miroslav and Marković, Zoran M. and Trajković, Vladimir S.",
year = "2010",
abstract = "The present study investigated the hemolytic properties of fullerene (C-60) nanoparticles prepared by solvent exchange using tetrahydrofuran (nC(60)THF), or by mechanochemically assisted complexation with macrocyclic oligosaccharide gamma-cyclodextrin (nC(60)CDX) or the copolymer ethylene vinyl acetate-ethylene vinyl versatate (nC(60)EVA-EVV). The spectrophotometrical analysis of hemoglobin release revealed that only nC(60)THF, but not nC(60)CDX or nC(60)EVA-EVV, was able to cause lysis of human erythrocytes in a dose-and time-dependent manner. Atomic force microscopy revealed that nC(60)THF-mediated hemolysis was preceded by erythrocyte shrinkage and increase in cell surface roughness. A flow cytometric analysis confirmed a decrease in erythrocyte size and demonstrated a significant increase in reactive oxygen species production in red blood cells exposed to nC(60)THF. The nC(60)THF-triggered hemolytic activity was efficiently reduced by the antioxidants N-acetylcysteine and butylated hydroxyanisole, as well as by serum albumin, the most abundant protein in human blood plasma. These data indicate that nC(60)THF can cause serum albumin-preventable hemolysis through oxidative stress-mediated damage of the erythrocyte membrane.",
journal = "Nanotechnology",
title = "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles",
volume = "21",
number = "37",
doi = "10.1088/0957-4484/21/37/375102"
}

Trpković, A., Todorović-Marković, B., Kleut, D., Misirkić, M., Janjetović, K. D., Vucicevic, L., Pantovic, A., Jovanović, S. P., Dramićanin, M., Marković, Z. M.,& Trajković, V. S.. (2010). Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology, 21(37).
https://doi.org/10.1088/0957-4484/21/37/375102

Trpković A, Todorović-Marković B, Kleut D, Misirkić M, Janjetović KD, Vucicevic L, Pantovic A, Jovanović SP, Dramićanin M, Marković ZM, Trajković VS. Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles. in Nanotechnology. 2010;21(37).
doi:10.1088/0957-4484/21/37/375102 .

Trpković, Andreja, Todorović-Marković, Biljana, Kleut, Duška, Misirkić, Maja, Janjetović, Kristina D., Vucicevic, Ljubica, Pantovic, Aleksandar, Jovanović, Svetlana P., Dramićanin, Miroslav, Marković, Zoran M., Trajković, Vladimir S., "Oxidative stress-mediated hemolytic activity of solvent exchange-prepared fullerene (C-60) nanoparticles" in Nanotechnology, 21, no. 37 (2010),
https://doi.org/10.1088/0957-4484/21/37/375102 . .