TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Guševac Stojanović, Ivana
AU  - Zarić, Marina
AU  - Martinović, Jelena
AU  - Mitrović, Nataša Lj.
AU  - Grković, Ivana
AU  - Drakulić, Dunja R.
PY  - 2020
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8742
AB  - Sustained activation of pro-apoptotic signaling due to a sudden and prolonged disturbance of cerebral blood circulation governs the neurodegenerative processes in prefrontal cortex (PFC) of rats whose common carotid arteries are permanently occluded. The adequate neuroprotective therapy should minimize the activation of toxicity pathways and increase the activity of endogenous protective mechanisms. Several neuroprotectants have been proposed, including progesterone (P4). However, the underlying mechanism of its action in PFC following permanent bilateral occlusion of common carotid arteries is not completely investigated. We, thus herein, tested the impact of post-ischemic P4 treatment (1.7 mg/kg for seven consecutive days) on previously reported aberrant neuronal morphology and amount of DNA fragmentation, as well as the expression of progesterone receptors along with the key elements of Akt/Erk/eNOS signal transduction pathway (Bax, Bcl-2, cytochrome C, caspase 3, PARP, and the level of nitric oxide). The obtained results indicate that potential amelioration of histological changes in PFC might be associated with the absence of activation of Bax/caspase 3 signaling cascade and the decline of DNA fragmentation. The study also provides the evidence that P4 treatment in repeated regiment of administration might be effective in neuronal protection against ischemic insult due to re-establishment of the compromised action of Akt/Erk/eNOS-mediated signaling pathway and the upregulation of progesterone receptors. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.
T2  - Cellular and Molecular Neurobiology
T1  - Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS
VL  - 40
IS  - 5
SP  - 829
EP  - 843
DO  - 10.1007/s10571-019-00777-2
ER  - 

@article{
author = "Stanojlović, Miloš R. and Guševac Stojanović, Ivana and Zarić, Marina and Martinović, Jelena and Mitrović, Nataša Lj. and Grković, Ivana and Drakulić, Dunja R.",
year = "2020",
abstract = "Sustained activation of pro-apoptotic signaling due to a sudden and prolonged disturbance of cerebral blood circulation governs the neurodegenerative processes in prefrontal cortex (PFC) of rats whose common carotid arteries are permanently occluded. The adequate neuroprotective therapy should minimize the activation of toxicity pathways and increase the activity of endogenous protective mechanisms. Several neuroprotectants have been proposed, including progesterone (P4). However, the underlying mechanism of its action in PFC following permanent bilateral occlusion of common carotid arteries is not completely investigated. We, thus herein, tested the impact of post-ischemic P4 treatment (1.7 mg/kg for seven consecutive days) on previously reported aberrant neuronal morphology and amount of DNA fragmentation, as well as the expression of progesterone receptors along with the key elements of Akt/Erk/eNOS signal transduction pathway (Bax, Bcl-2, cytochrome C, caspase 3, PARP, and the level of nitric oxide). The obtained results indicate that potential amelioration of histological changes in PFC might be associated with the absence of activation of Bax/caspase 3 signaling cascade and the decline of DNA fragmentation. The study also provides the evidence that P4 treatment in repeated regiment of administration might be effective in neuronal protection against ischemic insult due to re-establishment of the compromised action of Akt/Erk/eNOS-mediated signaling pathway and the upregulation of progesterone receptors. © 2019, Springer Science+Business Media, LLC, part of Springer Nature.",
journal = "Cellular and Molecular Neurobiology",
title = "Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS",
volume = "40",
number = "5",
pages = "829-843",
doi = "10.1007/s10571-019-00777-2"
}

Stanojlović, M. R., Guševac Stojanović, I., Zarić, M., Martinović, J., Mitrović, N. Lj., Grković, I.,& Drakulić, D. R.. (2020). Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS. in Cellular and Molecular Neurobiology, 40(5), 829-843.
https://doi.org/10.1007/s10571-019-00777-2

Stanojlović MR, Guševac Stojanović I, Zarić M, Martinović J, Mitrović NL, Grković I, Drakulić DR. Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS. in Cellular and Molecular Neurobiology. 2020;40(5):829-843.
doi:10.1007/s10571-019-00777-2 .

Stanojlović, Miloš R., Guševac Stojanović, Ivana, Zarić, Marina, Martinović, Jelena, Mitrović, Nataša Lj., Grković, Ivana, Drakulić, Dunja R., "Progesterone Protects Prefrontal Cortex in Rat Model of Permanent Bilateral Common Carotid Occlusion via Progesterone Receptors and Akt/Erk/eNOS" in Cellular and Molecular Neurobiology, 40, no. 5 (2020):829-843,
https://doi.org/10.1007/s10571-019-00777-2 . .

TY  - JOUR
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Drakulić, Dunja R.
AU  - Martinović, Jelena
AU  - Sevigny, Jean
AU  - Stanojlović, Miloš R.
AU  - Nedeljković, Nadežda
AU  - Grković, Ivana
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1459
AB  - 17 beta-Estradiol (E2) rapidly, by binding to membrane estrogen receptors, activates cell signaling cascades which induce formation of new dendritic spines in the hippocampus of males as in females, but the interaction with other metabolic processes, such as extracellular adenine nucleotides metabolism, are currently unknown. Extracellular adenine nucleotides play significant roles, controlling excitatory glutamatergic synapses and development of neural circuits and synaptic plasticity. Their precise regulation in the synaptic cleft is tightly controlled by ecto-nucleoside triphosphate diphosphohydrolase (NTPDase)/ecto-5-nucleotidase (eN) enzyme chain. Therefore, we sought to clarify whether a single systemic injection of E2 in male rats is accompanied by changes in the expression of the pre- and postsynaptic proteins and downstream kinases linked to E2-induced synaptic rearrangement as well as alterations in NTPDase/eN pathway in the hippocampal synaptosomes. Obtained data showed activation of mammalian target of rapamycin and upregulation of key synaptic proteins necessary for spine formation, 24 h after systemic E2 administration. In E2-mediated conditions, we found downregulation of NTPDase1 and NTPDase2 and attenuation of adenine nucleotide hydrolysis by NTPDase/eN enzyme chain, without changes in NTPDase3 properties and augmentation of synaptic tissue-nonspecific alkaline phosphatase (TNAP) activity. Despite reduced NTPDase activities, increased TNAP activity probably prevents toxic accumulation of ATP in the extracellular milieu and also hydrolyzes accumulated ADP due to unchanged NTPDase3 activity. Thus, our initial evaluation supports idea of specific roles of different ectonucleotidases and their coordinated actions in E2-mediated spine remodeling and maintenance.
T2  - Journal of Molecular Neuroscience
T1  - 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes
VL  - 61
IS  - 3
SP  - 412
EP  - 422
DO  - 10.1007/s12031-016-0877-6
ER  - 

@article{
author = "Mitrović, Nataša Lj. and Zarić, Marina and Drakulić, Dunja R. and Martinović, Jelena and Sevigny, Jean and Stanojlović, Miloš R. and Nedeljković, Nadežda and Grković, Ivana",
year = "2017",
abstract = "17 beta-Estradiol (E2) rapidly, by binding to membrane estrogen receptors, activates cell signaling cascades which induce formation of new dendritic spines in the hippocampus of males as in females, but the interaction with other metabolic processes, such as extracellular adenine nucleotides metabolism, are currently unknown. Extracellular adenine nucleotides play significant roles, controlling excitatory glutamatergic synapses and development of neural circuits and synaptic plasticity. Their precise regulation in the synaptic cleft is tightly controlled by ecto-nucleoside triphosphate diphosphohydrolase (NTPDase)/ecto-5-nucleotidase (eN) enzyme chain. Therefore, we sought to clarify whether a single systemic injection of E2 in male rats is accompanied by changes in the expression of the pre- and postsynaptic proteins and downstream kinases linked to E2-induced synaptic rearrangement as well as alterations in NTPDase/eN pathway in the hippocampal synaptosomes. Obtained data showed activation of mammalian target of rapamycin and upregulation of key synaptic proteins necessary for spine formation, 24 h after systemic E2 administration. In E2-mediated conditions, we found downregulation of NTPDase1 and NTPDase2 and attenuation of adenine nucleotide hydrolysis by NTPDase/eN enzyme chain, without changes in NTPDase3 properties and augmentation of synaptic tissue-nonspecific alkaline phosphatase (TNAP) activity. Despite reduced NTPDase activities, increased TNAP activity probably prevents toxic accumulation of ATP in the extracellular milieu and also hydrolyzes accumulated ADP due to unchanged NTPDase3 activity. Thus, our initial evaluation supports idea of specific roles of different ectonucleotidases and their coordinated actions in E2-mediated spine remodeling and maintenance.",
journal = "Journal of Molecular Neuroscience",
title = "17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes",
volume = "61",
number = "3",
pages = "412-422",
doi = "10.1007/s12031-016-0877-6"
}

Mitrović, N. Lj., Zarić, M., Drakulić, D. R., Martinović, J., Sevigny, J., Stanojlović, M. R., Nedeljković, N.,& Grković, I.. (2017). 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes. in Journal of Molecular Neuroscience, 61(3), 412-422.
https://doi.org/10.1007/s12031-016-0877-6

Mitrović NL, Zarić M, Drakulić DR, Martinović J, Sevigny J, Stanojlović MR, Nedeljković N, Grković I. 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes. in Journal of Molecular Neuroscience. 2017;61(3):412-422.
doi:10.1007/s12031-016-0877-6 .

Mitrović, Nataša Lj., Zarić, Marina, Drakulić, Dunja R., Martinović, Jelena, Sevigny, Jean, Stanojlović, Miloš R., Nedeljković, Nadežda, Grković, Ivana, "17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes" in Journal of Molecular Neuroscience, 61, no. 3 (2017):412-422,
https://doi.org/10.1007/s12031-016-0877-6 . .

TY  - JOUR
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Drakulić, Dunja R.
AU  - Martinović, Jelena
AU  - Sevigny, Jean
AU  - Stanojlović, Miloš R.
AU  - Nedeljković, Nadežda
AU  - Grković, Ivana
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1460
T2  - Journal of Molecular Neuroscience
T1  - Erratum to: 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes
VL  - 61
IS  - 3
SP  - 423
EP  - 424
DO  - 10.1007/s12031-016-0879-4
ER  - 

@article{
author = "Mitrović, Nataša Lj. and Zarić, Marina and Drakulić, Dunja R. and Martinović, Jelena and Sevigny, Jean and Stanojlović, Miloš R. and Nedeljković, Nadežda and Grković, Ivana",
year = "2017",
journal = "Journal of Molecular Neuroscience",
title = "Erratum to: 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes",
volume = "61",
number = "3",
pages = "423-424",
doi = "10.1007/s12031-016-0879-4"
}

Mitrović, N. Lj., Zarić, M., Drakulić, D. R., Martinović, J., Sevigny, J., Stanojlović, M. R., Nedeljković, N.,& Grković, I.. (2017). Erratum to: 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes. in Journal of Molecular Neuroscience, 61(3), 423-424.
https://doi.org/10.1007/s12031-016-0879-4

Mitrović NL, Zarić M, Drakulić DR, Martinović J, Sevigny J, Stanojlović MR, Nedeljković N, Grković I. Erratum to: 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes. in Journal of Molecular Neuroscience. 2017;61(3):423-424.
doi:10.1007/s12031-016-0879-4 .

Mitrović, Nataša Lj., Zarić, Marina, Drakulić, Dunja R., Martinović, Jelena, Sevigny, Jean, Stanojlović, Miloš R., Nedeljković, Nadežda, Grković, Ivana, "Erratum to: 17 beta-Estradiol-Induced Synaptic Rearrangements Are Accompanied by Altered Ectonucleotidase Activities in Male Rat Hippocampal Synaptosomes" in Journal of Molecular Neuroscience, 61, no. 3 (2017):423-424,
https://doi.org/10.1007/s12031-016-0879-4 . .

TY  - JOUR
AU  - Joksić, Gordana
AU  - Mićić, Mileva
AU  - Filipović, Jelena G.
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Calija, Bojan
AU  - Valenta-Šobot, Ana
AU  - Demajo, Miroslav
AU  - Nilsson, Robert
PY  - 2017
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1584
AB  - The study of cell proliferation is a useful tool in the fields of toxicology, pathophysiology and pharmacology. Cell proliferation and its degree can be evaluated using 5-bromo-2deoxyuridine which is incorporated into the newly synthesized DNA. The aim of this study was the optimization of subcutaneous application of 5-bromo-2-deoxyuridine implantation for continuous and persistent marking of proliferating cells in the rat forestomach. 3-tert-Butyl-4-hydroxyanisole was used as the agent that ensures cell proliferation. In order to determine the optimal dose for proliferating cells labeling, 5-bromo-2-deoxyuridine doses of 50 mg, 100 mg, 200 mg or 350 mg were implemented 2 days prior to sacrifice by flat-faced cylindrical matrices. Immunohistochemical analysis using 5-bromo-2-deoxyuridine in situ detection kit was performed for the detection of 5-bromo-2-deoxyuridine labeled cells. The results showed that for adult rats, the optimum 5-bromo-2-deoxyuridine dose is 200 mg per animal for subcutaneous application. The here described manner of 5-bromo-2-deoxyuridine in vivo labeling provides a simple, efficient, and reliable method for cell labeling, and at the same minimizes stress to animals.
T2  - Acta Veterinaria, Beograd
T1  - Cell Proliferation Assay - Method Optimisation for in Vivo Labeling of DNA in the Rat Forestomach
VL  - 67
IS  - 1
SP  - 1
EP  - 10
DO  - 10.1515/acve-2017-0001
ER  - 

@article{
author = "Joksić, Gordana and Mićić, Mileva and Filipović, Jelena G. and Drakulić, Dunja R. and Stanojlović, Miloš R. and Calija, Bojan and Valenta-Šobot, Ana and Demajo, Miroslav and Nilsson, Robert",
year = "2017",
abstract = "The study of cell proliferation is a useful tool in the fields of toxicology, pathophysiology and pharmacology. Cell proliferation and its degree can be evaluated using 5-bromo-2deoxyuridine which is incorporated into the newly synthesized DNA. The aim of this study was the optimization of subcutaneous application of 5-bromo-2-deoxyuridine implantation for continuous and persistent marking of proliferating cells in the rat forestomach. 3-tert-Butyl-4-hydroxyanisole was used as the agent that ensures cell proliferation. In order to determine the optimal dose for proliferating cells labeling, 5-bromo-2-deoxyuridine doses of 50 mg, 100 mg, 200 mg or 350 mg were implemented 2 days prior to sacrifice by flat-faced cylindrical matrices. Immunohistochemical analysis using 5-bromo-2-deoxyuridine in situ detection kit was performed for the detection of 5-bromo-2-deoxyuridine labeled cells. The results showed that for adult rats, the optimum 5-bromo-2-deoxyuridine dose is 200 mg per animal for subcutaneous application. The here described manner of 5-bromo-2-deoxyuridine in vivo labeling provides a simple, efficient, and reliable method for cell labeling, and at the same minimizes stress to animals.",
journal = "Acta Veterinaria, Beograd",
title = "Cell Proliferation Assay - Method Optimisation for in Vivo Labeling of DNA in the Rat Forestomach",
volume = "67",
number = "1",
pages = "1-10",
doi = "10.1515/acve-2017-0001"
}

Joksić, G., Mićić, M., Filipović, J. G., Drakulić, D. R., Stanojlović, M. R., Calija, B., Valenta-Šobot, A., Demajo, M.,& Nilsson, R.. (2017). Cell Proliferation Assay - Method Optimisation for in Vivo Labeling of DNA in the Rat Forestomach. in Acta Veterinaria, Beograd, 67(1), 1-10.
https://doi.org/10.1515/acve-2017-0001

Joksić G, Mićić M, Filipović JG, Drakulić DR, Stanojlović MR, Calija B, Valenta-Šobot A, Demajo M, Nilsson R. Cell Proliferation Assay - Method Optimisation for in Vivo Labeling of DNA in the Rat Forestomach. in Acta Veterinaria, Beograd. 2017;67(1):1-10.
doi:10.1515/acve-2017-0001 .

Joksić, Gordana, Mićić, Mileva, Filipović, Jelena G., Drakulić, Dunja R., Stanojlović, Miloš R., Calija, Bojan, Valenta-Šobot, Ana, Demajo, Miroslav, Nilsson, Robert, "Cell Proliferation Assay - Method Optimisation for in Vivo Labeling of DNA in the Rat Forestomach" in Acta Veterinaria, Beograd, 67, no. 1 (2017):1-10,
https://doi.org/10.1515/acve-2017-0001 . .

TY  - CONF
AU  - Guševac Stojanović, Ivana
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Grković, Ivana
AU  - Martinović, Jelena
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Veljković, Filip M.
AU  - Horvat, Anica
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9210
AB  - Reduction  of  oxygen  and  glucose  supply  to  the  brain  due  to  diminished cerebral  blood  flow  leads  to  damage  of  tissue  which  in  experimental conditions  can  be  mimicked  by  permanent  ligation  of  common  carotid arteries  (2VO).  Besides  numerous  genomic  and  non-genomic  processes, cerebral  ischemia  enhances  expression  of  ecto-5'-nucleotidase  (eN),  a  main enzyme  in  the  central  nervous  system  that  produces  potent  neuromodulator and neuroprotector, adenosine. Since progesterone (P), a potent sex steroid, is recognized as neuroprotective, aim of this study was to examine whether repeated  low-dose  P  treatment  is  capable  to  induce  changes  in  activity  and protein expression of eN, at rat cortical membrane fraction following 2VO. Obtained  results  indicate  that  P  modulates  investigated  parameters  and through  stimulation  of  adenosine  generation  might  promote  cytoprotection in ischemic brain.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2016 : 13th international conference on fundamental and applied aspects of physical chemistry
T1  - Progesterone upregulates activity and protein expression of efecto-5'-nucleotidase in ischemic brain of male wister rats
SP  - 455
EP  - 458
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9210
ER  - 

@conference{
author = "Guševac Stojanović, Ivana and Drakulić, Dunja R. and Stanojlović, Miloš R. and Grković, Ivana and Martinović, Jelena and Mitrović, Nataša Lj. and Zarić, Marina and Veljković, Filip M. and Horvat, Anica",
year = "2016",
abstract = "Reduction  of  oxygen  and  glucose  supply  to  the  brain  due  to  diminished cerebral  blood  flow  leads  to  damage  of  tissue  which  in  experimental conditions  can  be  mimicked  by  permanent  ligation  of  common  carotid arteries  (2VO).  Besides  numerous  genomic  and  non-genomic  processes, cerebral  ischemia  enhances  expression  of  ecto-5'-nucleotidase  (eN),  a  main enzyme  in  the  central  nervous  system  that  produces  potent  neuromodulator and neuroprotector, adenosine. Since progesterone (P), a potent sex steroid, is recognized as neuroprotective, aim of this study was to examine whether repeated  low-dose  P  treatment  is  capable  to  induce  changes  in  activity  and protein expression of eN, at rat cortical membrane fraction following 2VO. Obtained  results  indicate  that  P  modulates  investigated  parameters  and through  stimulation  of  adenosine  generation  might  promote  cytoprotection in ischemic brain.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2016 : 13th international conference on fundamental and applied aspects of physical chemistry",
title = "Progesterone upregulates activity and protein expression of efecto-5'-nucleotidase in ischemic brain of male wister rats",
pages = "455-458",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9210"
}

Guševac Stojanović, I., Drakulić, D. R., Stanojlović, M. R., Grković, I., Martinović, J., Mitrović, N. Lj., Zarić, M., Veljković, F. M.,& Horvat, A.. (2016). Progesterone upregulates activity and protein expression of efecto-5'-nucleotidase in ischemic brain of male wister rats. in Physical chemistry 2016 : 13th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 455-458.
https://hdl.handle.net/21.15107/rcub_vinar_9210

Guševac Stojanović I, Drakulić DR, Stanojlović MR, Grković I, Martinović J, Mitrović NL, Zarić M, Veljković FM, Horvat A. Progesterone upregulates activity and protein expression of efecto-5'-nucleotidase in ischemic brain of male wister rats. in Physical chemistry 2016 : 13th international conference on fundamental and applied aspects of physical chemistry. 2016;:455-458.
https://hdl.handle.net/21.15107/rcub_vinar_9210 .

Guševac Stojanović, Ivana, Drakulić, Dunja R., Stanojlović, Miloš R., Grković, Ivana, Martinović, Jelena, Mitrović, Nataša Lj., Zarić, Marina, Veljković, Filip M., Horvat, Anica, "Progesterone upregulates activity and protein expression of efecto-5'-nucleotidase in ischemic brain of male wister rats" in Physical chemistry 2016 : 13th international conference on fundamental and applied aspects of physical chemistry (2016):455-458,
https://hdl.handle.net/21.15107/rcub_vinar_9210 .

TY  - JOUR
AU  - Grković, Ivana
AU  - Bjelobaba, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Lavrnja, Irena
AU  - Drakulić, Dunja R.
AU  - Martinović, Jelena
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
AU  - Nedeljković, Nadežda
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1289
AB  - Nucleoside triphosphate diphosphohydrolase3 (NTPDase3) is membrane-bound ecto-enzyme which hydrolyzes extracellular ATP, thus modulating the function of purinergic receptors and the pattern of purinergic signaling. Here we analyzed the developmental expression of NTPDase3 in female hypothalamus, cerebral cortex and hippocampal formation at different postnatal ages (PD7-PD90) by qRT-PCR and immunohistochemistry. In hypothalamus and hippocampus, a similar developmental profile was seen: NTPDase3 gene expression was stable during postnatal development and increased in adults. In the cortex, upregulation of NTPDase3 mRNA expression was seen at PD15 and further increase was evidenced in adults. Immunohistochemical analysis at PD7 revealed faint neuronal NTPDase3 localization in a dorsal hypothalamus. The immunoreactivity (ir) gradually increased in PD15 and PD20, in clusters of cells in the lateral, ventral and dorsomedial hypothalamus. Furthermore, in PD20 animals, NTPDase3-ir was detected on short fibers in the posterior hypothalamic area, while in PD30 the fibers appeared progressively longer and markedly varicose. In adults, the strongest NTPDase3-ir was observed in collections of cells in dorsomedial hypothalamic nucleus, dorsal and lateral hypothalamus and in several thalamic areas, whereas the varicose fibers traversed entire diencephalon, particularly paraventricular thalamic nucleus, ventromedial and dorsomedial hypothalamic nuclei, the arcuate nucleus and the prefornical part of the lateral hypothalamus. The presumably ascending NTPDase3-ir fibers were first observed in PD20; their density and the varicose appearance increased until the adulthood. Prominent enhancement of NTPDase3-ir in the hypothalamus coincides with age when animals acquire diurnal rhythms of sleeping and feeding, supporting the hypothesis that this enzyme may be involved in regulation of homeostatic functions. (C) 2016 Elsevier B.V. All rights reserved.
T2  - Journal of Chemical Neuroanatomy
T1  - Expression of ecto-nucleoside triphosphate diphosphohydrolase3 (NTPDase3) in the female rat brain during postnatal development
VL  - 77
SP  - 10
EP  - 18
DO  - 10.1016/j.jchemneu.2016.04.001
ER  - 

@article{
author = "Grković, Ivana and Bjelobaba, Ivana and Mitrović, Nataša Lj. and Lavrnja, Irena and Drakulić, Dunja R. and Martinović, Jelena and Stanojlović, Miloš R. and Horvat, Anica and Nedeljković, Nadežda",
year = "2016",
abstract = "Nucleoside triphosphate diphosphohydrolase3 (NTPDase3) is membrane-bound ecto-enzyme which hydrolyzes extracellular ATP, thus modulating the function of purinergic receptors and the pattern of purinergic signaling. Here we analyzed the developmental expression of NTPDase3 in female hypothalamus, cerebral cortex and hippocampal formation at different postnatal ages (PD7-PD90) by qRT-PCR and immunohistochemistry. In hypothalamus and hippocampus, a similar developmental profile was seen: NTPDase3 gene expression was stable during postnatal development and increased in adults. In the cortex, upregulation of NTPDase3 mRNA expression was seen at PD15 and further increase was evidenced in adults. Immunohistochemical analysis at PD7 revealed faint neuronal NTPDase3 localization in a dorsal hypothalamus. The immunoreactivity (ir) gradually increased in PD15 and PD20, in clusters of cells in the lateral, ventral and dorsomedial hypothalamus. Furthermore, in PD20 animals, NTPDase3-ir was detected on short fibers in the posterior hypothalamic area, while in PD30 the fibers appeared progressively longer and markedly varicose. In adults, the strongest NTPDase3-ir was observed in collections of cells in dorsomedial hypothalamic nucleus, dorsal and lateral hypothalamus and in several thalamic areas, whereas the varicose fibers traversed entire diencephalon, particularly paraventricular thalamic nucleus, ventromedial and dorsomedial hypothalamic nuclei, the arcuate nucleus and the prefornical part of the lateral hypothalamus. The presumably ascending NTPDase3-ir fibers were first observed in PD20; their density and the varicose appearance increased until the adulthood. Prominent enhancement of NTPDase3-ir in the hypothalamus coincides with age when animals acquire diurnal rhythms of sleeping and feeding, supporting the hypothesis that this enzyme may be involved in regulation of homeostatic functions. (C) 2016 Elsevier B.V. All rights reserved.",
journal = "Journal of Chemical Neuroanatomy",
title = "Expression of ecto-nucleoside triphosphate diphosphohydrolase3 (NTPDase3) in the female rat brain during postnatal development",
volume = "77",
pages = "10-18",
doi = "10.1016/j.jchemneu.2016.04.001"
}

Grković, I., Bjelobaba, I., Mitrović, N. Lj., Lavrnja, I., Drakulić, D. R., Martinović, J., Stanojlović, M. R., Horvat, A.,& Nedeljković, N.. (2016). Expression of ecto-nucleoside triphosphate diphosphohydrolase3 (NTPDase3) in the female rat brain during postnatal development. in Journal of Chemical Neuroanatomy, 77, 10-18.
https://doi.org/10.1016/j.jchemneu.2016.04.001

Grković I, Bjelobaba I, Mitrović NL, Lavrnja I, Drakulić DR, Martinović J, Stanojlović MR, Horvat A, Nedeljković N. Expression of ecto-nucleoside triphosphate diphosphohydrolase3 (NTPDase3) in the female rat brain during postnatal development. in Journal of Chemical Neuroanatomy. 2016;77:10-18.
doi:10.1016/j.jchemneu.2016.04.001 .

Grković, Ivana, Bjelobaba, Ivana, Mitrović, Nataša Lj., Lavrnja, Irena, Drakulić, Dunja R., Martinović, Jelena, Stanojlović, Miloš R., Horvat, Anica, Nedeljković, Nadežda, "Expression of ecto-nucleoside triphosphate diphosphohydrolase3 (NTPDase3) in the female rat brain during postnatal development" in Journal of Chemical Neuroanatomy, 77 (2016):10-18,
https://doi.org/10.1016/j.jchemneu.2016.04.001 . .

TY  - JOUR
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Drakulić, Dunja R.
AU  - Martinović, Jelena
AU  - Stanojlović, Miloš R.
AU  - Sevigny, Jean
AU  - Horvat, Anica
AU  - Nedeljković, Nadežda
AU  - Grković, Ivana
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1022
AB  - 17 beta-Estradiol (E2) crucially affects several processes in the hippocampus of both sexes. E2 acts upon estradiol receptors ER alpha and ER beta, influencing target gene expression and/or modulates intracellular signaling cascades. Another potent modulator of hippocampal function is nucleoside adenosine, the final product of ectonucleoti-dase cascade, enzymes which hydrolyze extracellular ATP to adenosine. The last and rate-limiting step of the hydrolysis is catalyzed by membrane-bound ecto-50-nucleotidase (eN). Previous findings obtained on adenosine metabolism in brain suggest that eN may be modulated by ovarian steroids. Therefore, the present study reports that the activity and protein abundance of membrane-bound eN fluctuates across the estrus cycle in the hippocampal synaptosomes of female rats. Further, we analyzed the role of E2 and its intracellular receptors on the expression of eN in ovariectomized females. We found that E2 upregulated eN activity and protein abundance in the hippocampal synaptosomes. Application of nonspecific ER antagonist, ICI 182,780 and selective ERa and ERb agonists, PPT and DPN, respectively, demonstrated the involvement of both receptor subtypes in observed actions. Selective ERa receptor agonist, PPT, induced upregulation of both the protein level and activity of eN, while application of selective ERb receptor agonist, DPN, increased only the activity of eN. In both cases, E2 entered into the intracellular compartment and activated ER(s), which was demonstrated by membrane impermeable E2-BSA conjugate. Together these results imply that E2-induced effects on connectivity and functional properties of the hippocampal synapses may be in part mediated through observed effect on eN. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.
PB  - Elsevier
T2  - Neuroscience
T1  - 17 beta-ESTRADIOL UPREGULATES ECTO-5 -NUCLEOTIDASE (CD73) IN HIPPOCAMPAL SYNAPTOSOMES OF FEMALE RATS THROUGH ACTION MEDIATED BY ESTROGEN RECEPTOR-alpha AND -beta
VL  - 324
SP  - 286
EP  - 296
DO  - 10.1016/j.neuroscience.2016.03.022
ER  - 

@article{
author = "Mitrović, Nataša Lj. and Zarić, Marina and Drakulić, Dunja R. and Martinović, Jelena and Stanojlović, Miloš R. and Sevigny, Jean and Horvat, Anica and Nedeljković, Nadežda and Grković, Ivana",
year = "2016",
abstract = "17 beta-Estradiol (E2) crucially affects several processes in the hippocampus of both sexes. E2 acts upon estradiol receptors ER alpha and ER beta, influencing target gene expression and/or modulates intracellular signaling cascades. Another potent modulator of hippocampal function is nucleoside adenosine, the final product of ectonucleoti-dase cascade, enzymes which hydrolyze extracellular ATP to adenosine. The last and rate-limiting step of the hydrolysis is catalyzed by membrane-bound ecto-50-nucleotidase (eN). Previous findings obtained on adenosine metabolism in brain suggest that eN may be modulated by ovarian steroids. Therefore, the present study reports that the activity and protein abundance of membrane-bound eN fluctuates across the estrus cycle in the hippocampal synaptosomes of female rats. Further, we analyzed the role of E2 and its intracellular receptors on the expression of eN in ovariectomized females. We found that E2 upregulated eN activity and protein abundance in the hippocampal synaptosomes. Application of nonspecific ER antagonist, ICI 182,780 and selective ERa and ERb agonists, PPT and DPN, respectively, demonstrated the involvement of both receptor subtypes in observed actions. Selective ERa receptor agonist, PPT, induced upregulation of both the protein level and activity of eN, while application of selective ERb receptor agonist, DPN, increased only the activity of eN. In both cases, E2 entered into the intracellular compartment and activated ER(s), which was demonstrated by membrane impermeable E2-BSA conjugate. Together these results imply that E2-induced effects on connectivity and functional properties of the hippocampal synapses may be in part mediated through observed effect on eN. (C) 2016 IBRO. Published by Elsevier Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Neuroscience",
title = "17 beta-ESTRADIOL UPREGULATES ECTO-5 -NUCLEOTIDASE (CD73) IN HIPPOCAMPAL SYNAPTOSOMES OF FEMALE RATS THROUGH ACTION MEDIATED BY ESTROGEN RECEPTOR-alpha AND -beta",
volume = "324",
pages = "286-296",
doi = "10.1016/j.neuroscience.2016.03.022"
}

Mitrović, N. Lj., Zarić, M., Drakulić, D. R., Martinović, J., Stanojlović, M. R., Sevigny, J., Horvat, A., Nedeljković, N.,& Grković, I.. (2016). 17 beta-ESTRADIOL UPREGULATES ECTO-5 -NUCLEOTIDASE (CD73) IN HIPPOCAMPAL SYNAPTOSOMES OF FEMALE RATS THROUGH ACTION MEDIATED BY ESTROGEN RECEPTOR-alpha AND -beta. in Neuroscience
Elsevier., 324, 286-296.
https://doi.org/10.1016/j.neuroscience.2016.03.022

Mitrović NL, Zarić M, Drakulić DR, Martinović J, Stanojlović MR, Sevigny J, Horvat A, Nedeljković N, Grković I. 17 beta-ESTRADIOL UPREGULATES ECTO-5 -NUCLEOTIDASE (CD73) IN HIPPOCAMPAL SYNAPTOSOMES OF FEMALE RATS THROUGH ACTION MEDIATED BY ESTROGEN RECEPTOR-alpha AND -beta. in Neuroscience. 2016;324:286-296.
doi:10.1016/j.neuroscience.2016.03.022 .

Mitrović, Nataša Lj., Zarić, Marina, Drakulić, Dunja R., Martinović, Jelena, Stanojlović, Miloš R., Sevigny, Jean, Horvat, Anica, Nedeljković, Nadežda, Grković, Ivana, "17 beta-ESTRADIOL UPREGULATES ECTO-5 -NUCLEOTIDASE (CD73) IN HIPPOCAMPAL SYNAPTOSOMES OF FEMALE RATS THROUGH ACTION MEDIATED BY ESTROGEN RECEPTOR-alpha AND -beta" in Neuroscience, 324 (2016):286-296,
https://doi.org/10.1016/j.neuroscience.2016.03.022 . .

TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Guševac, Ivana
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Martinović, Jelena
AU  - Horvat, Anica
AU  - Drakulić, Dunja R.
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1156
AB  - Although a substantial number of pre-clinical and experimental studies have investigated effects of 17 beta-estradiol, its precise molecular mechanism of action in the early state of chronic cerebral hypoperfusion remains controversial. The present study attempted to verify whether post-ischemic estradiol treatment (33.3 mu g/kg for seven consecutive days) affects previously reported number of hippocampal apoptotic cells and amount of DNA fragmentation characteristic for apoptosis as well as the expression of key elements within synaptosomal Akt and Erk signal transduction pathways (NF-kappa B, Bax, Bcl-2, cytochrome C, caspase 3, and PARP). Additionally, alterations of aforementioned molecules linked to protection in various neurodegenerative disorders were monitored in the cytosolic, mitochondrial, and nuclear fractions associating investigated kinases and NF-kappa B with gene expression of their downstream effectors-Bcl-2, Bax, and caspase 3. The results revealed that an initial increase in the number of apoptotic cells and amount of DNA fragmentation induced by chronic cerebral hypoperfusion was significantly reduced by 17 beta-estradiol. In synaptic regions, an altered profile with respect to the protein expression of Bcl-2 and phosphorylated Akt was detected, although the level of other examined proteins was not modified. In other investigated sub-cellular fractions, 17 beta-estradiol elicited phosphorylation and translocation of Akt and Erk along with modulation of the expression of their subsequent effectors. Our findings support the concept that repeated post-ischemic 17 beta-estradiol treatment attenuates neurodegeneration induced by chronic cerebral hypoperfusion in hippocampus through the activation of investigated kinases and regulation of their downstream molecules in sub-cellular manner indicating a time window and regime of its administration as a valid therapeutic intervention.
T2  - Cellular and Molecular Neurobiology
T1  - Repeated Estradiol Treatment Attenuates Chronic Cerebral Hypoperfusion-Induced Neurodegeneration in Rat Hippocampus
VL  - 36
IS  - 6
SP  - 989
EP  - 999
DO  - 10.1007/s10571-015-0289-0
ER  - 

@article{
author = "Stanojlović, Miloš R. and Guševac, Ivana and Grković, Ivana and Mitrović, Nataša Lj. and Martinović, Jelena and Horvat, Anica and Drakulić, Dunja R.",
year = "2016",
abstract = "Although a substantial number of pre-clinical and experimental studies have investigated effects of 17 beta-estradiol, its precise molecular mechanism of action in the early state of chronic cerebral hypoperfusion remains controversial. The present study attempted to verify whether post-ischemic estradiol treatment (33.3 mu g/kg for seven consecutive days) affects previously reported number of hippocampal apoptotic cells and amount of DNA fragmentation characteristic for apoptosis as well as the expression of key elements within synaptosomal Akt and Erk signal transduction pathways (NF-kappa B, Bax, Bcl-2, cytochrome C, caspase 3, and PARP). Additionally, alterations of aforementioned molecules linked to protection in various neurodegenerative disorders were monitored in the cytosolic, mitochondrial, and nuclear fractions associating investigated kinases and NF-kappa B with gene expression of their downstream effectors-Bcl-2, Bax, and caspase 3. The results revealed that an initial increase in the number of apoptotic cells and amount of DNA fragmentation induced by chronic cerebral hypoperfusion was significantly reduced by 17 beta-estradiol. In synaptic regions, an altered profile with respect to the protein expression of Bcl-2 and phosphorylated Akt was detected, although the level of other examined proteins was not modified. In other investigated sub-cellular fractions, 17 beta-estradiol elicited phosphorylation and translocation of Akt and Erk along with modulation of the expression of their subsequent effectors. Our findings support the concept that repeated post-ischemic 17 beta-estradiol treatment attenuates neurodegeneration induced by chronic cerebral hypoperfusion in hippocampus through the activation of investigated kinases and regulation of their downstream molecules in sub-cellular manner indicating a time window and regime of its administration as a valid therapeutic intervention.",
journal = "Cellular and Molecular Neurobiology",
title = "Repeated Estradiol Treatment Attenuates Chronic Cerebral Hypoperfusion-Induced Neurodegeneration in Rat Hippocampus",
volume = "36",
number = "6",
pages = "989-999",
doi = "10.1007/s10571-015-0289-0"
}

Stanojlović, M. R., Guševac, I., Grković, I., Mitrović, N. Lj., Martinović, J., Horvat, A.,& Drakulić, D. R.. (2016). Repeated Estradiol Treatment Attenuates Chronic Cerebral Hypoperfusion-Induced Neurodegeneration in Rat Hippocampus. in Cellular and Molecular Neurobiology, 36(6), 989-999.
https://doi.org/10.1007/s10571-015-0289-0

Stanojlović MR, Guševac I, Grković I, Mitrović NL, Martinović J, Horvat A, Drakulić DR. Repeated Estradiol Treatment Attenuates Chronic Cerebral Hypoperfusion-Induced Neurodegeneration in Rat Hippocampus. in Cellular and Molecular Neurobiology. 2016;36(6):989-999.
doi:10.1007/s10571-015-0289-0 .

Stanojlović, Miloš R., Guševac, Ivana, Grković, Ivana, Mitrović, Nataša Lj., Martinović, Jelena, Horvat, Anica, Drakulić, Dunja R., "Repeated Estradiol Treatment Attenuates Chronic Cerebral Hypoperfusion-Induced Neurodegeneration in Rat Hippocampus" in Cellular and Molecular Neurobiology, 36, no. 6 (2016):989-999,
https://doi.org/10.1007/s10571-015-0289-0 . .

TY  - JOUR
AU  - Mitrović, Nataša Lj.
AU  - Guševac, Ivana
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Martinović, Jelena
AU  - Sevigny, Jean
AU  - Horvat, Anica
AU  - Nedeljković, Nadežda
AU  - Grković, Ivana
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1222
AB  - Ecto-5-nucleotidase (eN), a membrane rate-limiting enzyme of the purine catabolic pathway, catalyzes the conversion of AMP to adenosine involved in the regulation of many brain physiological and pathological processes. Since gender fundamentally determines hormonal milieu in the body and brain, it is reasonable to assume that sex differences in the activity of various signaling systems, including adenosine, may be generated by gonadal steroids. Thus, we examined expression of eN as a component of adenosine signaling system in the basal state in cerebral cortex and hippocampus of male and female rats at gene, protein and functional level, as well as in the state of gonadal hormone deprivation, induced by ovariectomy (OVX), whereas impact of steroid hormones was explored after repeated administration of 17 alpha-estradiol, 17 beta-estradiol and progesterone for seven consecutive days. Results showed regional and sex-related differences in basal eN activity level, with the highest AMP hydrolysis observed in the hippocampus of male rats. Furthermore, ovarian steroids do not contribute to basal gene eN expression or the activity in cortical and hippocampal region of female rats. However, protein eN expression was increased in OVX rats in both investigated region. Investigated exogenous steroids had no influence on eN expression in male brain, while in OVX females alterations in eN activity were induced. The observed effects in female rats were different between examined regions e.g. in cortex, applied treatments predominantly decreased whereas in hippocampus increased eN activity. Based on the presented results, eN exerts regional and sex-related response in basal state as well as after treatment with female gonadal hormones, however the exact mechanisms of sex steroids actions on eN remain unclear and should be fully explored. (C) 2016 Elsevier Inc. All rights reserved.
T2  - General and Comparative Endocrinology
T1  - Regional and sex-related differences in modulating effects of female sex steroids on ecto-5-nucleotidase expression in the rat cerebral cortex and hippocampus
VL  - 235
SP  - 100
EP  - 107
DO  - 10.1016/j.ygcen.2016.06.018
ER  - 

@article{
author = "Mitrović, Nataša Lj. and Guševac, Ivana and Drakulić, Dunja R. and Stanojlović, Miloš R. and Martinović, Jelena and Sevigny, Jean and Horvat, Anica and Nedeljković, Nadežda and Grković, Ivana",
year = "2016",
abstract = "Ecto-5-nucleotidase (eN), a membrane rate-limiting enzyme of the purine catabolic pathway, catalyzes the conversion of AMP to adenosine involved in the regulation of many brain physiological and pathological processes. Since gender fundamentally determines hormonal milieu in the body and brain, it is reasonable to assume that sex differences in the activity of various signaling systems, including adenosine, may be generated by gonadal steroids. Thus, we examined expression of eN as a component of adenosine signaling system in the basal state in cerebral cortex and hippocampus of male and female rats at gene, protein and functional level, as well as in the state of gonadal hormone deprivation, induced by ovariectomy (OVX), whereas impact of steroid hormones was explored after repeated administration of 17 alpha-estradiol, 17 beta-estradiol and progesterone for seven consecutive days. Results showed regional and sex-related differences in basal eN activity level, with the highest AMP hydrolysis observed in the hippocampus of male rats. Furthermore, ovarian steroids do not contribute to basal gene eN expression or the activity in cortical and hippocampal region of female rats. However, protein eN expression was increased in OVX rats in both investigated region. Investigated exogenous steroids had no influence on eN expression in male brain, while in OVX females alterations in eN activity were induced. The observed effects in female rats were different between examined regions e.g. in cortex, applied treatments predominantly decreased whereas in hippocampus increased eN activity. Based on the presented results, eN exerts regional and sex-related response in basal state as well as after treatment with female gonadal hormones, however the exact mechanisms of sex steroids actions on eN remain unclear and should be fully explored. (C) 2016 Elsevier Inc. All rights reserved.",
journal = "General and Comparative Endocrinology",
title = "Regional and sex-related differences in modulating effects of female sex steroids on ecto-5-nucleotidase expression in the rat cerebral cortex and hippocampus",
volume = "235",
pages = "100-107",
doi = "10.1016/j.ygcen.2016.06.018"
}

Mitrović, N. Lj., Guševac, I., Drakulić, D. R., Stanojlović, M. R., Martinović, J., Sevigny, J., Horvat, A., Nedeljković, N.,& Grković, I.. (2016). Regional and sex-related differences in modulating effects of female sex steroids on ecto-5-nucleotidase expression in the rat cerebral cortex and hippocampus. in General and Comparative Endocrinology, 235, 100-107.
https://doi.org/10.1016/j.ygcen.2016.06.018

Mitrović NL, Guševac I, Drakulić DR, Stanojlović MR, Martinović J, Sevigny J, Horvat A, Nedeljković N, Grković I. Regional and sex-related differences in modulating effects of female sex steroids on ecto-5-nucleotidase expression in the rat cerebral cortex and hippocampus. in General and Comparative Endocrinology. 2016;235:100-107.
doi:10.1016/j.ygcen.2016.06.018 .

Mitrović, Nataša Lj., Guševac, Ivana, Drakulić, Dunja R., Stanojlović, Miloš R., Martinović, Jelena, Sevigny, Jean, Horvat, Anica, Nedeljković, Nadežda, Grković, Ivana, "Regional and sex-related differences in modulating effects of female sex steroids on ecto-5-nucleotidase expression in the rat cerebral cortex and hippocampus" in General and Comparative Endocrinology, 235 (2016):100-107,
https://doi.org/10.1016/j.ygcen.2016.06.018 . .

TY  - JOUR
AU  - Nilsson, Robert
AU  - Mićić, Mileva
AU  - Filipović, Jelena G.
AU  - Valenta-Šobot, Ana
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Joksić, Gordana
PY  - 2016
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/1058
AB  - The aim of this study was to identify palatable additives which have a significant protective action against soft tissue changes in the oral cavity caused by Swedish smokeless tobacco (snus), and that satisfy existing legal requirements. Although the cancer risk from snus is extremely low, long term use may result in highly undesirable keratotic lesions and associated epithelial abnormalities in the oral cavity. The rat forestomach, which is vulnerable to the irritative action of non-genotoxic compounds like butylated hydroxyanisole, propionic acid as well as snus, was chosen as an experimental model. Studied toxicological endpoints included histopathology and cellular proliferation based on DNA incorporation of bromodeoxyuridine. After 6 weeks exposure, blueberries (bilberries) and an extract from the common milk thistle were found to exert a highly significant inhibition of cell proliferation induced by snus in the rat forestomach epithelium, indicating a potential protection with respect soft tissue changes in the human oral cavity. (C) 2016 Elsevier Inc. All rights reserved.
PB  - Elsevier
T2  - Regulatory Toxicology and Pharmacology
T1  - Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus)
VL  - 76
SP  - 94
EP  - 101
DO  - 10.1016/j.yrtph.2016.01.017
ER  - 

@article{
author = "Nilsson, Robert and Mićić, Mileva and Filipović, Jelena G. and Valenta-Šobot, Ana and Drakulić, Dunja R. and Stanojlović, Miloš R. and Joksić, Gordana",
year = "2016",
abstract = "The aim of this study was to identify palatable additives which have a significant protective action against soft tissue changes in the oral cavity caused by Swedish smokeless tobacco (snus), and that satisfy existing legal requirements. Although the cancer risk from snus is extremely low, long term use may result in highly undesirable keratotic lesions and associated epithelial abnormalities in the oral cavity. The rat forestomach, which is vulnerable to the irritative action of non-genotoxic compounds like butylated hydroxyanisole, propionic acid as well as snus, was chosen as an experimental model. Studied toxicological endpoints included histopathology and cellular proliferation based on DNA incorporation of bromodeoxyuridine. After 6 weeks exposure, blueberries (bilberries) and an extract from the common milk thistle were found to exert a highly significant inhibition of cell proliferation induced by snus in the rat forestomach epithelium, indicating a potential protection with respect soft tissue changes in the human oral cavity. (C) 2016 Elsevier Inc. All rights reserved.",
publisher = "Elsevier",
journal = "Regulatory Toxicology and Pharmacology",
title = "Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus)",
volume = "76",
pages = "94-101",
doi = "10.1016/j.yrtph.2016.01.017"
}

Nilsson, R., Mićić, M., Filipović, J. G., Valenta-Šobot, A., Drakulić, D. R., Stanojlović, M. R.,& Joksić, G.. (2016). Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus). in Regulatory Toxicology and Pharmacology
Elsevier., 76, 94-101.
https://doi.org/10.1016/j.yrtph.2016.01.017

Nilsson R, Mićić M, Filipović JG, Valenta-Šobot A, Drakulić DR, Stanojlović MR, Joksić G. Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus). in Regulatory Toxicology and Pharmacology. 2016;76:94-101.
doi:10.1016/j.yrtph.2016.01.017 .

Nilsson, Robert, Mićić, Mileva, Filipović, Jelena G., Valenta-Šobot, Ana, Drakulić, Dunja R., Stanojlović, Miloš R., Joksić, Gordana, "Inhibition by blueberries (bilberries) and extract from milk thistle of rat forestomach hyperplasia induced by oral smokeless tobacco (Swedish snus)" in Regulatory Toxicology and Pharmacology, 76 (2016):94-101,
https://doi.org/10.1016/j.yrtph.2016.01.017 . .

TY  - JOUR
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Nedeljković, Nadežda
AU  - Grković, Ivana
AU  - Velickovic, Natasa
AU  - Guševac, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Buzadzic, Ivana
AU  - Horvat, Anica
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/446
AB  - Although dexamethasone (DEX), a synthetic glucocorticoid receptor (GR) analog with profound effects on energy metabolism, immune system, and hypothalamic-pituitary-adrenal axis, is widely used therapeutically, its impact on the brain is poorly understood. The aim of the present study was to explore the effect of repeated low-dose DEX administration on the activity and expression of the ectonucleotidase enzymes which hydrolyze and therefore control extracellular ATP and adenosine concentrations in the synaptic cleft. Ectonucleotidases tested were ectonucleoside triphosphate diphosphohydrolase 1-3 (NTPDase1-3) and ecto-5-nucleotidase (eN), whereas the effects were evaluated in two brain areas that show different sensitivity to glucocorticoid action, hippocampus, and cerebral cortex. In the hippocampus, but not in cerebral cortex, modest level of neurodegenerative changes as well as increase in ATP, ADP, and AMP hydrolysis and upregulation of NTPDase1 and eN mRNA expression ensued under the influence of DEX. The observed pattern of ectonucleotidase activation, which creates tissue volume with enhanced capacity for adenosine formation, is the hallmark of the response after different insults to the brain.
T2  - Journal of Molecular Neuroscience
T1  - Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and Ecto-5-Nucleotidase in Rat Hippocampus after Repeated Low-Dose Dexamethasone Administration
VL  - 55
IS  - 4
SP  - 959
EP  - 967
DO  - 10.1007/s12031-014-0452-y
ER  - 

@article{
author = "Drakulić, Dunja R. and Stanojlović, Miloš R. and Nedeljković, Nadežda and Grković, Ivana and Velickovic, Natasa and Guševac, Ivana and Mitrović, Nataša Lj. and Buzadzic, Ivana and Horvat, Anica",
year = "2015",
abstract = "Although dexamethasone (DEX), a synthetic glucocorticoid receptor (GR) analog with profound effects on energy metabolism, immune system, and hypothalamic-pituitary-adrenal axis, is widely used therapeutically, its impact on the brain is poorly understood. The aim of the present study was to explore the effect of repeated low-dose DEX administration on the activity and expression of the ectonucleotidase enzymes which hydrolyze and therefore control extracellular ATP and adenosine concentrations in the synaptic cleft. Ectonucleotidases tested were ectonucleoside triphosphate diphosphohydrolase 1-3 (NTPDase1-3) and ecto-5-nucleotidase (eN), whereas the effects were evaluated in two brain areas that show different sensitivity to glucocorticoid action, hippocampus, and cerebral cortex. In the hippocampus, but not in cerebral cortex, modest level of neurodegenerative changes as well as increase in ATP, ADP, and AMP hydrolysis and upregulation of NTPDase1 and eN mRNA expression ensued under the influence of DEX. The observed pattern of ectonucleotidase activation, which creates tissue volume with enhanced capacity for adenosine formation, is the hallmark of the response after different insults to the brain.",
journal = "Journal of Molecular Neuroscience",
title = "Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and Ecto-5-Nucleotidase in Rat Hippocampus after Repeated Low-Dose Dexamethasone Administration",
volume = "55",
number = "4",
pages = "959-967",
doi = "10.1007/s12031-014-0452-y"
}

Drakulić, D. R., Stanojlović, M. R., Nedeljković, N., Grković, I., Velickovic, N., Guševac, I., Mitrović, N. Lj., Buzadzic, I.,& Horvat, A.. (2015). Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and Ecto-5-Nucleotidase in Rat Hippocampus after Repeated Low-Dose Dexamethasone Administration. in Journal of Molecular Neuroscience, 55(4), 959-967.
https://doi.org/10.1007/s12031-014-0452-y

Drakulić DR, Stanojlović MR, Nedeljković N, Grković I, Velickovic N, Guševac I, Mitrović NL, Buzadzic I, Horvat A. Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and Ecto-5-Nucleotidase in Rat Hippocampus after Repeated Low-Dose Dexamethasone Administration. in Journal of Molecular Neuroscience. 2015;55(4):959-967.
doi:10.1007/s12031-014-0452-y .

Drakulić, Dunja R., Stanojlović, Miloš R., Nedeljković, Nadežda, Grković, Ivana, Velickovic, Natasa, Guševac, Ivana, Mitrović, Nataša Lj., Buzadzic, Ivana, Horvat, Anica, "Upregulation of Nucleoside Triphosphate Diphosphohydrolase-1 and Ecto-5-Nucleotidase in Rat Hippocampus after Repeated Low-Dose Dexamethasone Administration" in Journal of Molecular Neuroscience, 55, no. 4 (2015):959-967,
https://doi.org/10.1007/s12031-014-0452-y . .

TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Martinović, Jelena
AU  - Guševac, Ivana
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Horvat, Anica
AU  - Drakulić, Dunja R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/527
AB  - Disturbance in blood circulation is associated with numerous pathological conditions characterized by cognitive decline and neurodegeneration. Activation of pro-apoptotic signaling previously detected in the synaptosomal fraction may underlie neurodegeneration in the prefrontal cortex of rats submitted to permanent bilateral common carotid arteries occlusion (two-vessel occlusion, 2VO). 17 beta-Estradiol (E) exerts potent neuroprotective effects in the brain affecting, among other, ischemia-induced pathological changes. As most significant changes in rats submitted to 2VO were observed on 7th day following the insult, of interest was to examine whether 7 day treatment with low dose of E (33.3 mu g/kg/day) prevents formerly reported neurodegeneration and may represent additional therapy during the early post-ischemic period. Role of E treatment on apoptotic pathway was monitored on Bcl-2 family members, cytochrome c, caspase 3 and PARP protein level in the synaptosomal (P2) fraction of the prefrontal cortex. Furthermore, changes of these proteins were examined in the cytosolic, mitochondrial and nuclear fraction, with the emphasis on potential involvement of extracellular signal-regulated kinases (ERK) and protein kinase B (Akt) activation and their role in nuclear translocation of transcriptional nuclear factor kappa B (NF-kB) associated with alteration of Box and Bcl-2 gene expression. The extent of cellular damage was determined using DNA fragmentation and Fluoro-Jade B staining. The absence of activation of apoptotic cascade both in the P2 and cell accompanied with decreased DNA fragmentation and number of degenerating neurons clearly indicates that E treatment ensures the efficient protection against ischemic insult. Moreover, E-mediated modulation of pro-apoptotic signaling in the cortical cellular fractions involves cooperative activation of ERK and Akt, which may be implicated in the observed prevention of neurodegenerative changes. (C) 2015 Elsevier Ltd. All rights reserved.
T2  - Neurochemistry International
T1  - Repeated low-dose 17 beta-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia
VL  - 83-84
SP  - 1
EP  - 8
DO  - 10.1016/j.neuint.2015.03.002
ER  - 

@article{
author = "Stanojlović, Miloš R. and Martinović, Jelena and Guševac, Ivana and Grković, Ivana and Mitrović, Nataša Lj. and Zarić, Marina and Horvat, Anica and Drakulić, Dunja R.",
year = "2015",
abstract = "Disturbance in blood circulation is associated with numerous pathological conditions characterized by cognitive decline and neurodegeneration. Activation of pro-apoptotic signaling previously detected in the synaptosomal fraction may underlie neurodegeneration in the prefrontal cortex of rats submitted to permanent bilateral common carotid arteries occlusion (two-vessel occlusion, 2VO). 17 beta-Estradiol (E) exerts potent neuroprotective effects in the brain affecting, among other, ischemia-induced pathological changes. As most significant changes in rats submitted to 2VO were observed on 7th day following the insult, of interest was to examine whether 7 day treatment with low dose of E (33.3 mu g/kg/day) prevents formerly reported neurodegeneration and may represent additional therapy during the early post-ischemic period. Role of E treatment on apoptotic pathway was monitored on Bcl-2 family members, cytochrome c, caspase 3 and PARP protein level in the synaptosomal (P2) fraction of the prefrontal cortex. Furthermore, changes of these proteins were examined in the cytosolic, mitochondrial and nuclear fraction, with the emphasis on potential involvement of extracellular signal-regulated kinases (ERK) and protein kinase B (Akt) activation and their role in nuclear translocation of transcriptional nuclear factor kappa B (NF-kB) associated with alteration of Box and Bcl-2 gene expression. The extent of cellular damage was determined using DNA fragmentation and Fluoro-Jade B staining. The absence of activation of apoptotic cascade both in the P2 and cell accompanied with decreased DNA fragmentation and number of degenerating neurons clearly indicates that E treatment ensures the efficient protection against ischemic insult. Moreover, E-mediated modulation of pro-apoptotic signaling in the cortical cellular fractions involves cooperative activation of ERK and Akt, which may be implicated in the observed prevention of neurodegenerative changes. (C) 2015 Elsevier Ltd. All rights reserved.",
journal = "Neurochemistry International",
title = "Repeated low-dose 17 beta-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia",
volume = "83-84",
pages = "1-8",
doi = "10.1016/j.neuint.2015.03.002"
}

Stanojlović, M. R., Martinović, J., Guševac, I., Grković, I., Mitrović, N. Lj., Zarić, M., Horvat, A.,& Drakulić, D. R.. (2015). Repeated low-dose 17 beta-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia. in Neurochemistry International, 83-84, 1-8.
https://doi.org/10.1016/j.neuint.2015.03.002

Stanojlović MR, Martinović J, Guševac I, Grković I, Mitrović NL, Zarić M, Horvat A, Drakulić DR. Repeated low-dose 17 beta-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia. in Neurochemistry International. 2015;83-84:1-8.
doi:10.1016/j.neuint.2015.03.002 .

Stanojlović, Miloš R., Martinović, Jelena, Guševac, Ivana, Grković, Ivana, Mitrović, Nataša Lj., Zarić, Marina, Horvat, Anica, Drakulić, Dunja R., "Repeated low-dose 17 beta-estradiol treatment prevents activation of apoptotic signaling both in the synaptosomal and cellular fraction in rat prefrontal cortex following cerebral ischemia" in Neurochemistry International, 83-84 (2015):1-8,
https://doi.org/10.1016/j.neuint.2015.03.002 . .

TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Guševac, Ivana
AU  - Grković, Ivana
AU  - Martinović, Jelena
AU  - Mitrović, Nataša Lj.
AU  - Zarić, Marina
AU  - Horvat, Anica
AU  - Drakulić, Dunja R.
PY  - 2015
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/846
AB  - The present study attempted to investigate how chronic cerebral hypoperfusion (CCH) and repeated low-dose progesterone (P) treatment affect gene and protein expression, subcellular distribution of key apoptotic elements within protein kinase B (Akt) and extracellular signal-regulated kinases (Erk) signal transduction pathways, as well as neurodegenerative processes and behavior. The results revealed the absence of Erk activation in CCH in cytosolic and synaptosomal fractions, indicating a lower threshold of Akt activation in brain ischemia, while P increased their levels above control values. CCH induced an increase in caspase 3 (Casp 3) and poly (ADP-ribose) polymerase (PARP) gene and protein expression. However, P restored expression of examined molecules in all observed fractions, except for the levels of Casp 3 in synapses which highlighted its possible non-apoptotic or even protective function. Our study showed the absence of nuclear factor kappa-light-chain-enhancer of activated b cells (NF-kappa B) response to this type of ischemic condition and its strong activation under the influence of P. Further, the initial increase in the number of apoptotic cells and amount of DNA fragmentation induced by CCH was significantly reduced by P. Finally, P reversed the CCH-induced reduction in locomotor activity, while promoting a substantial decrease in anxiety-related behavior. Our findings support the concept that repeated low-dose post-ischemic P treatment reduces CCH-induced neurodegeneration in the hippocampus. Neuroprotection is initiated through the activation of investigated kinases and regulation of their downstream molecules in subcellular specific manner, indicating that this treatment may be a promising therapy for alleviation of CCH-induced pathologies. (C) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.
PB  - Elsevier
T2  - Neuroscience
T1  - Effects of Chronic Cerebral Hypoperfusion and Low-Dose Progesterone Treatment on Apoptotic Processes, Expression and Subcellular Localization of Key Elements Within Akt and Erk Signaling Pathways in Rat Hippocampus
VL  - 311
SP  - 308
EP  - 321
DO  - 10.1016/j.neuroscience.2015.10.040
ER  - 

@article{
author = "Stanojlović, Miloš R. and Guševac, Ivana and Grković, Ivana and Martinović, Jelena and Mitrović, Nataša Lj. and Zarić, Marina and Horvat, Anica and Drakulić, Dunja R.",
year = "2015",
abstract = "The present study attempted to investigate how chronic cerebral hypoperfusion (CCH) and repeated low-dose progesterone (P) treatment affect gene and protein expression, subcellular distribution of key apoptotic elements within protein kinase B (Akt) and extracellular signal-regulated kinases (Erk) signal transduction pathways, as well as neurodegenerative processes and behavior. The results revealed the absence of Erk activation in CCH in cytosolic and synaptosomal fractions, indicating a lower threshold of Akt activation in brain ischemia, while P increased their levels above control values. CCH induced an increase in caspase 3 (Casp 3) and poly (ADP-ribose) polymerase (PARP) gene and protein expression. However, P restored expression of examined molecules in all observed fractions, except for the levels of Casp 3 in synapses which highlighted its possible non-apoptotic or even protective function. Our study showed the absence of nuclear factor kappa-light-chain-enhancer of activated b cells (NF-kappa B) response to this type of ischemic condition and its strong activation under the influence of P. Further, the initial increase in the number of apoptotic cells and amount of DNA fragmentation induced by CCH was significantly reduced by P. Finally, P reversed the CCH-induced reduction in locomotor activity, while promoting a substantial decrease in anxiety-related behavior. Our findings support the concept that repeated low-dose post-ischemic P treatment reduces CCH-induced neurodegeneration in the hippocampus. Neuroprotection is initiated through the activation of investigated kinases and regulation of their downstream molecules in subcellular specific manner, indicating that this treatment may be a promising therapy for alleviation of CCH-induced pathologies. (C) 2015 IBRO. Published by Elsevier Ltd. All rights reserved.",
publisher = "Elsevier",
journal = "Neuroscience",
title = "Effects of Chronic Cerebral Hypoperfusion and Low-Dose Progesterone Treatment on Apoptotic Processes, Expression and Subcellular Localization of Key Elements Within Akt and Erk Signaling Pathways in Rat Hippocampus",
volume = "311",
pages = "308-321",
doi = "10.1016/j.neuroscience.2015.10.040"
}

Stanojlović, M. R., Guševac, I., Grković, I., Martinović, J., Mitrović, N. Lj., Zarić, M., Horvat, A.,& Drakulić, D. R.. (2015). Effects of Chronic Cerebral Hypoperfusion and Low-Dose Progesterone Treatment on Apoptotic Processes, Expression and Subcellular Localization of Key Elements Within Akt and Erk Signaling Pathways in Rat Hippocampus. in Neuroscience
Elsevier., 311, 308-321.
https://doi.org/10.1016/j.neuroscience.2015.10.040

Stanojlović MR, Guševac I, Grković I, Martinović J, Mitrović NL, Zarić M, Horvat A, Drakulić DR. Effects of Chronic Cerebral Hypoperfusion and Low-Dose Progesterone Treatment on Apoptotic Processes, Expression and Subcellular Localization of Key Elements Within Akt and Erk Signaling Pathways in Rat Hippocampus. in Neuroscience. 2015;311:308-321.
doi:10.1016/j.neuroscience.2015.10.040 .

Stanojlović, Miloš R., Guševac, Ivana, Grković, Ivana, Martinović, Jelena, Mitrović, Nataša Lj., Zarić, Marina, Horvat, Anica, Drakulić, Dunja R., "Effects of Chronic Cerebral Hypoperfusion and Low-Dose Progesterone Treatment on Apoptotic Processes, Expression and Subcellular Localization of Key Elements Within Akt and Erk Signaling Pathways in Rat Hippocampus" in Neuroscience, 311 (2015):308-321,
https://doi.org/10.1016/j.neuroscience.2015.10.040 . .

TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
AU  - Guševac, Ivana
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Buzadzic, I.
AU  - Drakulić, Dunja R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5445
AB  - To study time-dependent and gender-specific intracellular and biochemical mechanisms that lead to neurodegeneration due to moderate but persistent reduction of cerebral blood flow, adult male and female Wistar rats were divided into two main groups controls that underwent sham operation and animals subjected to permanent bilateral occlusion of common carotid arteries. Animals were sacrificed 3, 7 or 90 days following the insult. Expression of several apoptotic proteins in synaptic fractions along with Fluoro-Jade B staining and DNA fragmentation assay were used to estimate the apoptotic processes and potential neurodegeneration in cerebral cortex. Data suggest a time-specific increase of Bax as well as time- and gender-associated down-regulation in protein expression of Bcl-2, up-regulation of procaspase 3, accompanied with increased cleavage of procaspase 3 and PARP in synaptic terminals. Furthermore, time- but not gender-specific neurodegeneration was observed. Our findings support the concept of time- and gender-associated response to permanent bilateral occlusion of common carotid arteries, which would enable better understanding of the mechanisms underlying cerebral hypoperfusion.
T2  - Folia Biologica
T1  - Time Course of Cerebral Hypoperfusion-Induced Neurodegenerative Changes in the Cortex of Male and Female Rats
VL  - 60
IS  - 3
SP  - 123
EP  - 132
UR  - https://hdl.handle.net/21.15107/rcub_vinar_5445
ER  - 

@article{
author = "Stanojlović, Miloš R. and Horvat, Anica and Guševac, Ivana and Grković, Ivana and Mitrović, Nataša Lj. and Buzadzic, I. and Drakulić, Dunja R.",
year = "2014",
abstract = "To study time-dependent and gender-specific intracellular and biochemical mechanisms that lead to neurodegeneration due to moderate but persistent reduction of cerebral blood flow, adult male and female Wistar rats were divided into two main groups controls that underwent sham operation and animals subjected to permanent bilateral occlusion of common carotid arteries. Animals were sacrificed 3, 7 or 90 days following the insult. Expression of several apoptotic proteins in synaptic fractions along with Fluoro-Jade B staining and DNA fragmentation assay were used to estimate the apoptotic processes and potential neurodegeneration in cerebral cortex. Data suggest a time-specific increase of Bax as well as time- and gender-associated down-regulation in protein expression of Bcl-2, up-regulation of procaspase 3, accompanied with increased cleavage of procaspase 3 and PARP in synaptic terminals. Furthermore, time- but not gender-specific neurodegeneration was observed. Our findings support the concept of time- and gender-associated response to permanent bilateral occlusion of common carotid arteries, which would enable better understanding of the mechanisms underlying cerebral hypoperfusion.",
journal = "Folia Biologica",
title = "Time Course of Cerebral Hypoperfusion-Induced Neurodegenerative Changes in the Cortex of Male and Female Rats",
volume = "60",
number = "3",
pages = "123-132",
url = "https://hdl.handle.net/21.15107/rcub_vinar_5445"
}

Stanojlović, M. R., Horvat, A., Guševac, I., Grković, I., Mitrović, N. Lj., Buzadzic, I.,& Drakulić, D. R.. (2014). Time Course of Cerebral Hypoperfusion-Induced Neurodegenerative Changes in the Cortex of Male and Female Rats. in Folia Biologica, 60(3), 123-132.
https://hdl.handle.net/21.15107/rcub_vinar_5445

Stanojlović MR, Horvat A, Guševac I, Grković I, Mitrović NL, Buzadzic I, Drakulić DR. Time Course of Cerebral Hypoperfusion-Induced Neurodegenerative Changes in the Cortex of Male and Female Rats. in Folia Biologica. 2014;60(3):123-132.
https://hdl.handle.net/21.15107/rcub_vinar_5445 .

Stanojlović, Miloš R., Horvat, Anica, Guševac, Ivana, Grković, Ivana, Mitrović, Nataša Lj., Buzadzic, I., Drakulić, Dunja R., "Time Course of Cerebral Hypoperfusion-Induced Neurodegenerative Changes in the Cortex of Male and Female Rats" in Folia Biologica, 60, no. 3 (2014):123-132,
https://hdl.handle.net/21.15107/rcub_vinar_5445 .

TY  - THES
AU  - Stanojlović, Miloš R.
PY  - 2014
UR  - http://eteze.bg.ac.rs/application/showtheses?thesesId=2839
UR  - https://fedorabg.bg.ac.rs/fedora/get/o:11044/bdef:Content/download
UR  - http://vbs.rs/scripts/cobiss?command=DISPLAY&base=99999&RID=1024769714
UR  - http://nardus.mpn.gov.rs/123456789/5281
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/8089
AB  - Iako se ishemijske bolesti mozga, koje se karakterišu pogoršanjem motornih i kognitivnih funkcija, uključujući smanjenje sposobnosti učenja i memorije, intenzivno proučavaju poslednjih 20 godina malo je poznato o molekulskim mehanizmima njihovog nastanka,  (...)
AB  - Although ischemic brain diseases, characterized by decline of motor and cognitive functions, including reducing the ability of learning and memory, have been intensively studied over the past 20 years, the molecular mechanisms of their generation, as well  (...)
PB  - Универзитет у Београду, Биолошки факултет
T2  - Универзитет у Београду
T1  - Efekat estradiola u modulaciji apoptotskih signala u moždanoj kori i hipokampusu pacova tokom hronične moždane hipoperfuzije
T1  - Effects of estradiol on modulation of apoptotic signals in cerebral cortex and hippocampus of rats during chronic cerebral hypoperfusion
UR  - https://hdl.handle.net/21.15107/rcub_nardus_5281
ER  - 

@phdthesis{
author = "Stanojlović, Miloš R.",
year = "2014",
abstract = "Iako se ishemijske bolesti mozga, koje se karakterišu pogoršanjem motornih i kognitivnih funkcija, uključujući smanjenje sposobnosti učenja i memorije, intenzivno proučavaju poslednjih 20 godina malo je poznato o molekulskim mehanizmima njihovog nastanka,  (...), Although ischemic brain diseases, characterized by decline of motor and cognitive functions, including reducing the ability of learning and memory, have been intensively studied over the past 20 years, the molecular mechanisms of their generation, as well  (...)",
publisher = "Универзитет у Београду, Биолошки факултет",
journal = "Универзитет у Београду",
title = "Efekat estradiola u modulaciji apoptotskih signala u moždanoj kori i hipokampusu pacova tokom hronične moždane hipoperfuzije, Effects of estradiol on modulation of apoptotic signals in cerebral cortex and hippocampus of rats during chronic cerebral hypoperfusion",
url = "https://hdl.handle.net/21.15107/rcub_nardus_5281"
}

Stanojlović, M. R.. (2014). Efekat estradiola u modulaciji apoptotskih signala u moždanoj kori i hipokampusu pacova tokom hronične moždane hipoperfuzije. in Универзитет у Београду
Универзитет у Београду, Биолошки факултет..
https://hdl.handle.net/21.15107/rcub_nardus_5281

Stanojlović MR. Efekat estradiola u modulaciji apoptotskih signala u moždanoj kori i hipokampusu pacova tokom hronične moždane hipoperfuzije. in Универзитет у Београду. 2014;.
https://hdl.handle.net/21.15107/rcub_nardus_5281 .

Stanojlović, Miloš R., "Efekat estradiola u modulaciji apoptotskih signala u moždanoj kori i hipokampusu pacova tokom hronične moždane hipoperfuzije" in Универзитет у Београду (2014),
https://hdl.handle.net/21.15107/rcub_nardus_5281 .

TY  - JOUR
AU  - Grković, Ivana
AU  - Bjelobaba, Ivana
AU  - Nedeljković, Nadežda
AU  - Mitrović, Nataša Lj.
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/64
AB  - Ecto-5-nucleotidase (e-5NT), a glycosylphosphatidylinositol-linked membrane protein, catalyzes a conversion of AMP to adenosine, which influences nearly every aspect of brain physiology, including embryonic and postnatal brain development. The present study aimed to investigate a pattern of expression, activity and kinetic properties of e-5NT in the hippocampal formation and synaptic plasma membrane (SPM) preparations in rats at postnatal days (PDs) 7, 15, 20, 30 and 90. By combining gene expression analysis and enzyme histochemistry, we observed that e-5NT mRNA reached the adult level at PD20, while the enzyme activity continued to increase beyond this age. Further analysis revealed that hippocampal layers rich in synapses expressed the highest levels of e-5NT activity, while in layers populated with neuronal cell bodies, the enzyme activity was weak or absent. Therefore, activity and expression of e-5NT were analyzed in SPM preparations isolated from rats at different ages. The presence of two protein bands of about 65 and 68 kDa was determined by immunoblot analysis. The 65-kDa band was present at all ages, and its abundance increased from PD7 to PD20. The 68-kDa band appeared at PD15 and increased until PD30, coinciding with the increase of e-5NT activity, substrate affinity and enzymatic efficiency. Since distinct e-5NT isoforms may derive from different patterns of the enzyme protein N-glycosylation, we speculate that long-term regulation of e-5NT activity in adulthood may be effectuated at posttranslational level and without overall change in the gene and protein expression.
T2  - Journal of Molecular Neuroscience
T1  - Developmental Increase in Ecto-5-Nucleotidase Activity Overlaps with Appearance of Two Immunologically Distinct Enzyme Isoforms in Rat Hippocampal Synaptic Plasma Membranes
VL  - 54
IS  - 1
SP  - 109
EP  - 118
DO  - 10.1007/s12031-014-0256-0
ER  - 

@article{
author = "Grković, Ivana and Bjelobaba, Ivana and Nedeljković, Nadežda and Mitrović, Nataša Lj. and Drakulić, Dunja R. and Stanojlović, Miloš R. and Horvat, Anica",
year = "2014",
abstract = "Ecto-5-nucleotidase (e-5NT), a glycosylphosphatidylinositol-linked membrane protein, catalyzes a conversion of AMP to adenosine, which influences nearly every aspect of brain physiology, including embryonic and postnatal brain development. The present study aimed to investigate a pattern of expression, activity and kinetic properties of e-5NT in the hippocampal formation and synaptic plasma membrane (SPM) preparations in rats at postnatal days (PDs) 7, 15, 20, 30 and 90. By combining gene expression analysis and enzyme histochemistry, we observed that e-5NT mRNA reached the adult level at PD20, while the enzyme activity continued to increase beyond this age. Further analysis revealed that hippocampal layers rich in synapses expressed the highest levels of e-5NT activity, while in layers populated with neuronal cell bodies, the enzyme activity was weak or absent. Therefore, activity and expression of e-5NT were analyzed in SPM preparations isolated from rats at different ages. The presence of two protein bands of about 65 and 68 kDa was determined by immunoblot analysis. The 65-kDa band was present at all ages, and its abundance increased from PD7 to PD20. The 68-kDa band appeared at PD15 and increased until PD30, coinciding with the increase of e-5NT activity, substrate affinity and enzymatic efficiency. Since distinct e-5NT isoforms may derive from different patterns of the enzyme protein N-glycosylation, we speculate that long-term regulation of e-5NT activity in adulthood may be effectuated at posttranslational level and without overall change in the gene and protein expression.",
journal = "Journal of Molecular Neuroscience",
title = "Developmental Increase in Ecto-5-Nucleotidase Activity Overlaps with Appearance of Two Immunologically Distinct Enzyme Isoforms in Rat Hippocampal Synaptic Plasma Membranes",
volume = "54",
number = "1",
pages = "109-118",
doi = "10.1007/s12031-014-0256-0"
}

Grković, I., Bjelobaba, I., Nedeljković, N., Mitrović, N. Lj., Drakulić, D. R., Stanojlović, M. R.,& Horvat, A.. (2014). Developmental Increase in Ecto-5-Nucleotidase Activity Overlaps with Appearance of Two Immunologically Distinct Enzyme Isoforms in Rat Hippocampal Synaptic Plasma Membranes. in Journal of Molecular Neuroscience, 54(1), 109-118.
https://doi.org/10.1007/s12031-014-0256-0

Grković I, Bjelobaba I, Nedeljković N, Mitrović NL, Drakulić DR, Stanojlović MR, Horvat A. Developmental Increase in Ecto-5-Nucleotidase Activity Overlaps with Appearance of Two Immunologically Distinct Enzyme Isoforms in Rat Hippocampal Synaptic Plasma Membranes. in Journal of Molecular Neuroscience. 2014;54(1):109-118.
doi:10.1007/s12031-014-0256-0 .

Grković, Ivana, Bjelobaba, Ivana, Nedeljković, Nadežda, Mitrović, Nataša Lj., Drakulić, Dunja R., Stanojlović, Miloš R., Horvat, Anica, "Developmental Increase in Ecto-5-Nucleotidase Activity Overlaps with Appearance of Two Immunologically Distinct Enzyme Isoforms in Rat Hippocampal Synaptic Plasma Membranes" in Journal of Molecular Neuroscience, 54, no. 1 (2014):109-118,
https://doi.org/10.1007/s12031-014-0256-0 . .

TY  - JOUR
AU  - Stanojlović, Miloš R.
AU  - Guševac, Ivana
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Horvat, Anica
AU  - Drakulić, Dunja R.
PY  - 2014
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/301
AB  - Although the model of cerebral hypoperfusion in rats has been a matter of many investigations over the years, the exact intracellular and biochemical mechanisms that lead to neuron loss and memory decline have not been clearly identified. In the current study, we examined whether cerebral hypoperfusion causes changes in hippocampal protein expression of apoptotic markers in the synaptosomal fraction and neurodegeneration in a time-dependent and sex-specific manner. Adult male and female Wistar rats were divided into two main groups, controls that underwent sham operation, and animals subjected to permanent bilateral occlusion of common carotid arteries. Both male and female rats were killed 3, 7 or 90 days following the insult. The obtained results indicate that the peak of processes that lead to apoptosis occured on postoperative day 7 and that they were more prominent in males, indicating that neuroprotective effects of certain substances (planned for future experiments), should be tested at this time point.
T2  - Archives of Biological Sciences
T1  - Time-Related Sex Diffrences in Cerebral Hypoperfusion-Induced Brain Injury
VL  - 66
IS  - 4
SP  - 1673
EP  - 1680
DO  - 10.2298/ABS1404673S
ER  - 

@article{
author = "Stanojlović, Miloš R. and Guševac, Ivana and Grković, Ivana and Mitrović, Nataša Lj. and Horvat, Anica and Drakulić, Dunja R.",
year = "2014",
abstract = "Although the model of cerebral hypoperfusion in rats has been a matter of many investigations over the years, the exact intracellular and biochemical mechanisms that lead to neuron loss and memory decline have not been clearly identified. In the current study, we examined whether cerebral hypoperfusion causes changes in hippocampal protein expression of apoptotic markers in the synaptosomal fraction and neurodegeneration in a time-dependent and sex-specific manner. Adult male and female Wistar rats were divided into two main groups, controls that underwent sham operation, and animals subjected to permanent bilateral occlusion of common carotid arteries. Both male and female rats were killed 3, 7 or 90 days following the insult. The obtained results indicate that the peak of processes that lead to apoptosis occured on postoperative day 7 and that they were more prominent in males, indicating that neuroprotective effects of certain substances (planned for future experiments), should be tested at this time point.",
journal = "Archives of Biological Sciences",
title = "Time-Related Sex Diffrences in Cerebral Hypoperfusion-Induced Brain Injury",
volume = "66",
number = "4",
pages = "1673-1680",
doi = "10.2298/ABS1404673S"
}

Stanojlović, M. R., Guševac, I., Grković, I., Mitrović, N. Lj., Horvat, A.,& Drakulić, D. R.. (2014). Time-Related Sex Diffrences in Cerebral Hypoperfusion-Induced Brain Injury. in Archives of Biological Sciences, 66(4), 1673-1680.
https://doi.org/10.2298/ABS1404673S

Stanojlović MR, Guševac I, Grković I, Mitrović NL, Horvat A, Drakulić DR. Time-Related Sex Diffrences in Cerebral Hypoperfusion-Induced Brain Injury. in Archives of Biological Sciences. 2014;66(4):1673-1680.
doi:10.2298/ABS1404673S .

Stanojlović, Miloš R., Guševac, Ivana, Grković, Ivana, Mitrović, Nataša Lj., Horvat, Anica, Drakulić, Dunja R., "Time-Related Sex Diffrences in Cerebral Hypoperfusion-Induced Brain Injury" in Archives of Biological Sciences, 66, no. 4 (2014):1673-1680,
https://doi.org/10.2298/ABS1404673S . .

TY  - JOUR
AU  - Drakulić, Dunja R.
AU  - Velickovic, N.
AU  - Stanojlović, Miloš R.
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Lavrnja, I.
AU  - Horvat, Anica
PY  - 2013
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5549
AB  - Synthetic glucocorticoid dexamethasone (DEX), a highly potent anti-inflammatory and immunosuppressive agent, is widely used in the treatment of brain cancer, as well as for inflammatory and autoimmune diseases. The present study aimed to determine whether low-dose subchronic DEX treatment (100g/kg for eight consecutive days) exerts long-term effects on apoptosis in the adult rat prefrontal cortex (PFC) by examining the expression of cell death-promoting molecules [poly(ADP-ribose) polymerase (PARP), p53, procaspase 3, cleaved caspase 3, Bax] and cell-survival molecules (AKT, Bcl-2). The results obtained revealed that body, thymus and adrenal gland weights, as well corticosterone levels, in the serum and PFC were reduced 1day after the last DEX injection. In the PFC, DEX caused activation of AKT, augmentation of pro-survival Bcl-2 protein and an enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to the mitochondria. An unaltered profile with respect to the protein expression of apoptotic molecules PARP, procaspase 3 and Bax was detected, whereas p53 protein was decreased. Reverse transcriptase -polymerase chain reaction analysis showed a decrease of p53 mRNA levels and no significant difference in Bcl-2 and Bax mRNA expression in DEX-treated rats. Finally, a DNA fragmentation assay and Fluoro-Jade staining demonstrated no considerable changes in apoptosis in the rat PFC. Our findings support the concept that low-dose DEX creates a hypocorticoid state in the brain and also indicate that subchronic DEX treatment activates the pro-survival signalling pathway but does not change apoptotic markers in the rat PFC. This mechanism might be relevant for the DEX-induced apoptosis resistance observed during and after chemotherapy of patients with brain tumours.
T2  - Journal of Neuroendocrinology
T1  - Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex
VL  - 25
IS  - 7
SP  - 605
EP  - 616
DO  - 10.1111/jne.12037
ER  - 

@article{
author = "Drakulić, Dunja R. and Velickovic, N. and Stanojlović, Miloš R. and Grković, Ivana and Mitrović, Nataša Lj. and Lavrnja, I. and Horvat, Anica",
year = "2013",
abstract = "Synthetic glucocorticoid dexamethasone (DEX), a highly potent anti-inflammatory and immunosuppressive agent, is widely used in the treatment of brain cancer, as well as for inflammatory and autoimmune diseases. The present study aimed to determine whether low-dose subchronic DEX treatment (100g/kg for eight consecutive days) exerts long-term effects on apoptosis in the adult rat prefrontal cortex (PFC) by examining the expression of cell death-promoting molecules [poly(ADP-ribose) polymerase (PARP), p53, procaspase 3, cleaved caspase 3, Bax] and cell-survival molecules (AKT, Bcl-2). The results obtained revealed that body, thymus and adrenal gland weights, as well corticosterone levels, in the serum and PFC were reduced 1day after the last DEX injection. In the PFC, DEX caused activation of AKT, augmentation of pro-survival Bcl-2 protein and an enhanced Bcl-2/Bax protein ratio, as well Bcl-2 translocation to the mitochondria. An unaltered profile with respect to the protein expression of apoptotic molecules PARP, procaspase 3 and Bax was detected, whereas p53 protein was decreased. Reverse transcriptase -polymerase chain reaction analysis showed a decrease of p53 mRNA levels and no significant difference in Bcl-2 and Bax mRNA expression in DEX-treated rats. Finally, a DNA fragmentation assay and Fluoro-Jade staining demonstrated no considerable changes in apoptosis in the rat PFC. Our findings support the concept that low-dose DEX creates a hypocorticoid state in the brain and also indicate that subchronic DEX treatment activates the pro-survival signalling pathway but does not change apoptotic markers in the rat PFC. This mechanism might be relevant for the DEX-induced apoptosis resistance observed during and after chemotherapy of patients with brain tumours.",
journal = "Journal of Neuroendocrinology",
title = "Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex",
volume = "25",
number = "7",
pages = "605-616",
doi = "10.1111/jne.12037"
}

Drakulić, D. R., Velickovic, N., Stanojlović, M. R., Grković, I., Mitrović, N. Lj., Lavrnja, I.,& Horvat, A.. (2013). Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex. in Journal of Neuroendocrinology, 25(7), 605-616.
https://doi.org/10.1111/jne.12037

Drakulić DR, Velickovic N, Stanojlović MR, Grković I, Mitrović NL, Lavrnja I, Horvat A. Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex. in Journal of Neuroendocrinology. 2013;25(7):605-616.
doi:10.1111/jne.12037 .

Drakulić, Dunja R., Velickovic, N., Stanojlović, Miloš R., Grković, Ivana, Mitrović, Nataša Lj., Lavrnja, I., Horvat, Anica, "Low-Dose Dexamethasone Treatment Promotes the Pro-Survival Signalling Pathway in the Adult Rat Prefrontal Cortex" in Journal of Neuroendocrinology, 25, no. 7 (2013):605-616,
https://doi.org/10.1111/jne.12037 . .

TY  - JOUR
AU  - Petrović, Snježana
AU  - Milošević, Maja
AU  - Drakulić, Dunja R.
AU  - Grković, Ivana
AU  - Stanojlović, Miloš R.
AU  - Mitrović, Nataša Lj.
AU  - Horvat, Anica
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5012
AB  - The aim of this study was to examine the rapid non-genomic effect of 17 beta-estradiol (E2) on Ca2+ transport in mitochondria isolated from the nerve terminals (synaptosomes) of caudate nuclei (NC) and brain stems (BS) of ovariectomised female rats. In physiological conditions no effect of E2 on Ca2+ influx into synaptosomal mitochondria through ruthenium red (RR)-sensitive uniporter was observed. However, in the presence of uncoupling agent carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mu mol/l), pre-treatment with 0.5 nmol/l E2 protected mitochondrial membrane potential and consequently increased Ca2+ influx (2.3-fold in NC and 3.1-fold in BS). At the same time, 0.5 nmol/l E2 by increasing the affinity of mitochondrial Na+/Ca2+ exchanger for Na+ inhibited mitochondrial Ca2+ efflux in NC and BS by about 40%. Also, the specific binding of physiological E2 concentrations (0.1-10 nmol/l) to isolated synaptosomal mitochondria was detected. Using membrane impermeable E2 bound to bovine serum albumin and selective inhibitor of mitochondrial Na+/Ca2+ exchanger, we obtained that E2s action on mitochondrial Ca2+ efflux at least partially is due to the direct effects on the mitochondrial membrane and/or Na+/Ca2+ exchanger located in inner mitochondrial membrane. Our results implicate E2 as a modulator of Ca2+ concentration in mitochondrial matrix, and ultimately in the cytosol. Given the vital role of Ca2+ in regulation of total nerve cells activity, especially energy metabolism, neurotransmission and directing the cells toward survival or cell death, the effects on mitochondrial Ca2+ transport could be one of the important modes of E2 neuromodulatory action independent of the genome. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.
T2  - Neuroscience
T1  - 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem
VL  - 220
SP  - 32
EP  - 40
DO  - 10.1016/j.neuroscience.2012.06.040
ER  - 

@article{
author = "Petrović, Snježana and Milošević, Maja and Drakulić, Dunja R. and Grković, Ivana and Stanojlović, Miloš R. and Mitrović, Nataša Lj. and Horvat, Anica",
year = "2012",
abstract = "The aim of this study was to examine the rapid non-genomic effect of 17 beta-estradiol (E2) on Ca2+ transport in mitochondria isolated from the nerve terminals (synaptosomes) of caudate nuclei (NC) and brain stems (BS) of ovariectomised female rats. In physiological conditions no effect of E2 on Ca2+ influx into synaptosomal mitochondria through ruthenium red (RR)-sensitive uniporter was observed. However, in the presence of uncoupling agent carbonyl cyanide4-(trifluoromethoxy)phenylhydrazone (FCCP) (1 mu mol/l), pre-treatment with 0.5 nmol/l E2 protected mitochondrial membrane potential and consequently increased Ca2+ influx (2.3-fold in NC and 3.1-fold in BS). At the same time, 0.5 nmol/l E2 by increasing the affinity of mitochondrial Na+/Ca2+ exchanger for Na+ inhibited mitochondrial Ca2+ efflux in NC and BS by about 40%. Also, the specific binding of physiological E2 concentrations (0.1-10 nmol/l) to isolated synaptosomal mitochondria was detected. Using membrane impermeable E2 bound to bovine serum albumin and selective inhibitor of mitochondrial Na+/Ca2+ exchanger, we obtained that E2s action on mitochondrial Ca2+ efflux at least partially is due to the direct effects on the mitochondrial membrane and/or Na+/Ca2+ exchanger located in inner mitochondrial membrane. Our results implicate E2 as a modulator of Ca2+ concentration in mitochondrial matrix, and ultimately in the cytosol. Given the vital role of Ca2+ in regulation of total nerve cells activity, especially energy metabolism, neurotransmission and directing the cells toward survival or cell death, the effects on mitochondrial Ca2+ transport could be one of the important modes of E2 neuromodulatory action independent of the genome. (C) 2012 IBRO. Published by Elsevier Ltd. All rights reserved.",
journal = "Neuroscience",
title = "17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem",
volume = "220",
pages = "32-40",
doi = "10.1016/j.neuroscience.2012.06.040"
}

Petrović, S., Milošević, M., Drakulić, D. R., Grković, I., Stanojlović, M. R., Mitrović, N. Lj.,& Horvat, A.. (2012). 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem. in Neuroscience, 220, 32-40.
https://doi.org/10.1016/j.neuroscience.2012.06.040

Petrović S, Milošević M, Drakulić DR, Grković I, Stanojlović MR, Mitrović NL, Horvat A. 17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem. in Neuroscience. 2012;220:32-40.
doi:10.1016/j.neuroscience.2012.06.040 .

Petrović, Snježana, Milošević, Maja, Drakulić, Dunja R., Grković, Ivana, Stanojlović, Miloš R., Mitrović, Nataša Lj., Horvat, Anica, "17 beta-estradiol modulates mitochondrial Ca2+ flux in rat caudate nucleus and brain stem" in Neuroscience, 220 (2012):32-40,
https://doi.org/10.1016/j.neuroscience.2012.06.040 . .

TY  - JOUR
AU  - Velickovic, Natasa
AU  - Drakulić, Dunja R.
AU  - Petrovic, Snjezana
AU  - Grković, Ivana
AU  - Milošević, Maja
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/5051
AB  - Recent studies reported that exposure of juvenile rats to cranial irradiation affects hypothalamic-pituitary-adrenal (HPA) axis stability, leading to its activation along with radiation-induced inflammation. In the present study, we hypothesized whether inflammatory reaction in the CNS could be a mediator of HPA axis response to cranial irradiation (CI). Therefore, we analyzed time-course changes of serum corticosterone level, as well IL-1 beta and TNF-alpha level in the serum and hypothalamus of juvenile rats after CI. Protein and gene expression of the glucocorticoid receptor (GR) and nuclear factor kappaB (NF kappa B) were examined in the hippocampus within 24 h postirradiation interval. Cranial irradiation led to rapid induction of both GR and NF kappa B mRNA and protein in the hippocampus at 1 h. The increment in NF kappa B protein persisted for 2 h, therefore NF kappa B/GR protein ratio was turned in favor of NF kappa B. Central inflammation was characterized by increased IL-1 beta in the hypothalamus, with maximum levels at 2 and 4 h after irradiation, while both IL-1 beta and TNF-alpha were undetectable in the serum. Enhanced hypothalamic IL-1 beta probably induced the relocation of hippocampal NF kappa B to the nucleus and decreased NF kappa B mRNA at 6 h, indicating promotion of inflammation in the key tissue for HPA axis regulation. Concomitant increase of corticosterone level and enhanced GR nuclear translocation in the hippocampus at 6 h might represent a compensatory mechanism for observed inflammation. Our results indicate that acute radiation response is characterized by increased central inflammation and concomitant HPA axis activation, most likely having a role in protection of the organism from overwhelming inflammatory reaction.
T2  - Cellular and Molecular Neurobiology
T1  - Time-Course of Hypothalamic-Pituitary-Adrenal Axis Activity and Inflammation in Juvenile Rat Brain After Cranial Irradiation
VL  - 32
IS  - 7
SP  - 1175
EP  - 1185
DO  - 10.1007/s10571-012-9843-1
ER  - 

@article{
author = "Velickovic, Natasa and Drakulić, Dunja R. and Petrovic, Snjezana and Grković, Ivana and Milošević, Maja and Stanojlović, Miloš R. and Horvat, Anica",
year = "2012",
abstract = "Recent studies reported that exposure of juvenile rats to cranial irradiation affects hypothalamic-pituitary-adrenal (HPA) axis stability, leading to its activation along with radiation-induced inflammation. In the present study, we hypothesized whether inflammatory reaction in the CNS could be a mediator of HPA axis response to cranial irradiation (CI). Therefore, we analyzed time-course changes of serum corticosterone level, as well IL-1 beta and TNF-alpha level in the serum and hypothalamus of juvenile rats after CI. Protein and gene expression of the glucocorticoid receptor (GR) and nuclear factor kappaB (NF kappa B) were examined in the hippocampus within 24 h postirradiation interval. Cranial irradiation led to rapid induction of both GR and NF kappa B mRNA and protein in the hippocampus at 1 h. The increment in NF kappa B protein persisted for 2 h, therefore NF kappa B/GR protein ratio was turned in favor of NF kappa B. Central inflammation was characterized by increased IL-1 beta in the hypothalamus, with maximum levels at 2 and 4 h after irradiation, while both IL-1 beta and TNF-alpha were undetectable in the serum. Enhanced hypothalamic IL-1 beta probably induced the relocation of hippocampal NF kappa B to the nucleus and decreased NF kappa B mRNA at 6 h, indicating promotion of inflammation in the key tissue for HPA axis regulation. Concomitant increase of corticosterone level and enhanced GR nuclear translocation in the hippocampus at 6 h might represent a compensatory mechanism for observed inflammation. Our results indicate that acute radiation response is characterized by increased central inflammation and concomitant HPA axis activation, most likely having a role in protection of the organism from overwhelming inflammatory reaction.",
journal = "Cellular and Molecular Neurobiology",
title = "Time-Course of Hypothalamic-Pituitary-Adrenal Axis Activity and Inflammation in Juvenile Rat Brain After Cranial Irradiation",
volume = "32",
number = "7",
pages = "1175-1185",
doi = "10.1007/s10571-012-9843-1"
}

Velickovic, N., Drakulić, D. R., Petrovic, S., Grković, I., Milošević, M., Stanojlović, M. R.,& Horvat, A.. (2012). Time-Course of Hypothalamic-Pituitary-Adrenal Axis Activity and Inflammation in Juvenile Rat Brain After Cranial Irradiation. in Cellular and Molecular Neurobiology, 32(7), 1175-1185.
https://doi.org/10.1007/s10571-012-9843-1

Velickovic N, Drakulić DR, Petrovic S, Grković I, Milošević M, Stanojlović MR, Horvat A. Time-Course of Hypothalamic-Pituitary-Adrenal Axis Activity and Inflammation in Juvenile Rat Brain After Cranial Irradiation. in Cellular and Molecular Neurobiology. 2012;32(7):1175-1185.
doi:10.1007/s10571-012-9843-1 .

Velickovic, Natasa, Drakulić, Dunja R., Petrovic, Snjezana, Grković, Ivana, Milošević, Maja, Stanojlović, Miloš R., Horvat, Anica, "Time-Course of Hypothalamic-Pituitary-Adrenal Axis Activity and Inflammation in Juvenile Rat Brain After Cranial Irradiation" in Cellular and Molecular Neurobiology, 32, no. 7 (2012):1175-1185,
https://doi.org/10.1007/s10571-012-9843-1 . .

TY  - CONF
AU  - Drakulić, Dunja R.
AU  - Grković, Ivana
AU  - Milošević, Maja
AU  - Petrović, Snježana
AU  - Stanojlović, Miloš R.
AU  - Mitrović, Nataša Lj.
AU  - Horvat, Anica
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9295
AB  - The present study was performed to investigate whether acute whole-body exposure of
female adult rats to low dose (0.5 Gy) of ionizing irradiation (IR) is sufficient to alter
ectonucleotidase enzyme activities in the brain. All measurements were done at time
points 1, 24 and 72h after irradiation. Neuronal synaptic plasma membranes (SPMs)
were isolated from whole brains and enzyme activities were determined by monitoring
ATP, ADP and AMP hydrolysis in vitro. Our results indicate that whole-body IR is
able to modulate investigated brain enzyme activities in a time-dependent manner.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
T1  - Radiation-mediated modulations of extracelluar nucleotide hydrolysis in adult female rat brain
VL  - 1
SP  - 373
EP  - 375
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9295
ER  - 

@conference{
author = "Drakulić, Dunja R. and Grković, Ivana and Milošević, Maja and Petrović, Snježana and Stanojlović, Miloš R. and Mitrović, Nataša Lj. and Horvat, Anica",
year = "2012",
abstract = "The present study was performed to investigate whether acute whole-body exposure of
female adult rats to low dose (0.5 Gy) of ionizing irradiation (IR) is sufficient to alter
ectonucleotidase enzyme activities in the brain. All measurements were done at time
points 1, 24 and 72h after irradiation. Neuronal synaptic plasma membranes (SPMs)
were isolated from whole brains and enzyme activities were determined by monitoring
ATP, ADP and AMP hydrolysis in vitro. Our results indicate that whole-body IR is
able to modulate investigated brain enzyme activities in a time-dependent manner.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry",
title = "Radiation-mediated modulations of extracelluar nucleotide hydrolysis in adult female rat brain",
volume = "1",
pages = "373-375",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9295"
}

Drakulić, D. R., Grković, I., Milošević, M., Petrović, S., Stanojlović, M. R., Mitrović, N. Lj.,& Horvat, A.. (2012). Radiation-mediated modulations of extracelluar nucleotide hydrolysis in adult female rat brain. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 1, 373-375.
https://hdl.handle.net/21.15107/rcub_vinar_9295

Drakulić DR, Grković I, Milošević M, Petrović S, Stanojlović MR, Mitrović NL, Horvat A. Radiation-mediated modulations of extracelluar nucleotide hydrolysis in adult female rat brain. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry. 2012;1:373-375.
https://hdl.handle.net/21.15107/rcub_vinar_9295 .

Drakulić, Dunja R., Grković, Ivana, Milošević, Maja, Petrović, Snježana, Stanojlović, Miloš R., Mitrović, Nataša Lj., Horvat, Anica, "Radiation-mediated modulations of extracelluar nucleotide hydrolysis in adult female rat brain" in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry, 1 (2012):373-375,
https://hdl.handle.net/21.15107/rcub_vinar_9295 .

TY  - CONF
AU  - Stanojlović, Miloš R.
AU  - Drakulić, Dunja R.
AU  - Grković, Ivana
AU  - Mitrović, Nataša Lj.
AU  - Horvat, Anica
PY  - 2012
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/9296
AB  - Model of permanent bilateral occlusion of common carotid arteries (2VO) is generally
used to investigate mechanisms of chronic cerebral hypoperfusion that occurs in aging
and other neurodegenerative processes. The aim of this study was to determine timedependent modulation of mitochondrial apoptotic signaling in cortical brain area
following chronic cerebral hypoperfusion. Using Western blot technique we monitored
the changes in the expression of proteins of Bcl-2 family (Bcl-2, Bax) 3, 7 and 90 days
following the insult. According to our results the greatest impact of chronic cerebral
hipoperfusion occurred on 7th day.
PB  - Society of Physical Chemists of Serbia
C3  - Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
T1  - Time-dependent expression of Bcl-2 and Bax proteins in cortical brain area of adult wistar rats after permanent bilateral occlusions
VL  - 1
SP  - 376
EP  - 378
UR  - https://hdl.handle.net/21.15107/rcub_vinar_9296
ER  - 

@conference{
author = "Stanojlović, Miloš R. and Drakulić, Dunja R. and Grković, Ivana and Mitrović, Nataša Lj. and Horvat, Anica",
year = "2012",
abstract = "Model of permanent bilateral occlusion of common carotid arteries (2VO) is generally
used to investigate mechanisms of chronic cerebral hypoperfusion that occurs in aging
and other neurodegenerative processes. The aim of this study was to determine timedependent modulation of mitochondrial apoptotic signaling in cortical brain area
following chronic cerebral hypoperfusion. Using Western blot technique we monitored
the changes in the expression of proteins of Bcl-2 family (Bcl-2, Bax) 3, 7 and 90 days
following the insult. According to our results the greatest impact of chronic cerebral
hipoperfusion occurred on 7th day.",
publisher = "Society of Physical Chemists of Serbia",
journal = "Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry",
title = "Time-dependent expression of Bcl-2 and Bax proteins in cortical brain area of adult wistar rats after permanent bilateral occlusions",
volume = "1",
pages = "376-378",
url = "https://hdl.handle.net/21.15107/rcub_vinar_9296"
}

Stanojlović, M. R., Drakulić, D. R., Grković, I., Mitrović, N. Lj.,& Horvat, A.. (2012). Time-dependent expression of Bcl-2 and Bax proteins in cortical brain area of adult wistar rats after permanent bilateral occlusions. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry
Society of Physical Chemists of Serbia., 1, 376-378.
https://hdl.handle.net/21.15107/rcub_vinar_9296

Stanojlović MR, Drakulić DR, Grković I, Mitrović NL, Horvat A. Time-dependent expression of Bcl-2 and Bax proteins in cortical brain area of adult wistar rats after permanent bilateral occlusions. in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry. 2012;1:376-378.
https://hdl.handle.net/21.15107/rcub_vinar_9296 .

Stanojlović, Miloš R., Drakulić, Dunja R., Grković, Ivana, Mitrović, Nataša Lj., Horvat, Anica, "Time-dependent expression of Bcl-2 and Bax proteins in cortical brain area of adult wistar rats after permanent bilateral occlusions" in Physical chemistry 2012 : 11th international conference on fundamental and applied aspects of physical chemistry, 1 (2012):376-378,
https://hdl.handle.net/21.15107/rcub_vinar_9296 .

TY  - JOUR
AU  - Petrović, S.
AU  - Velickovic, N.
AU  - Stanojević, Ivana
AU  - Milošević, Maja
AU  - Drakulić, Dunja R.
AU  - Stanojlović, Miloš R.
AU  - Horvat, Anica
PY  - 2011
UR  - https://vinar.vin.bg.ac.rs/handle/123456789/4512
AB  - Our results, as well as those of others, have indicated that 17 beta-estradiol (E2) exerts its nongenomic effects in neuronal cells by affecting plasma membrane Ca2+ flux. In neuronal cells mitochondria possess Ca2+ buffering properties as they both sequester and release Ca2+. The goal of this study was to examine the rapid non-genomic effect of E2 on mitochondria! Ca2+ transport in hippocampal synaptosomes from ovariectomised rats. In addition, we aimed to determine if, and to what extent, E2 receptors participated in mitochondria! Ca2+ transport modulation by E2 in vitro. E2-specific binding and Ca2+ transport was monitored. At physiological E2 concentrations (0.1-1.5 nmol/L), specific E2 binding to mitochondria isolated from hippocampal synaptosomes was detected with a B-max and K-m of 37.6 +/- 2.6 fmol/mg protein and 0.69 +/- 0.14 nmol/L of free E2, respectively. The main mitochondrial Ca2+ influx mechanism is the Ruthenium Red-sensitive uniporter driven by mitochondrial membrane potential. Despite no effect of E2 on Ca2+ influx, a physiological E2 concentration (0.5 nmol/L) protected mitochondrial membrane potential and consequently Ca2+ influx from the uncoupling agent carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (1 mu mol/L). In neuronal cells the predominant mitochondria! Ca2+ efflux mechanism is the Na+/Ca2+ exchanger. E2 caused Ca2+ efflux inhibition (by 46%) coupled with increased affinity of the Na+/Ca2+ exchanger for Na+. Using E2 receptor (ER alpha and ER beta) antagonists and agonists, we confirmed ER betas involvement in E2-induced mitochondrial membrane potential protection as well as Ca2+ efflux inhibition. In summary, our results indicate that the nongenomic neuromodulatory role of E2 in rat hippocampus is achieved by affecting mitochondria! Ca2+ transport via, in part, mitochondrial ER beta. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.
T2  - Neuroscience
T1  - Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus
VL  - 192
SP  - 195
EP  - 204
DO  - 10.1016/j.neuroscience.2011.06.030
ER  - 

@article{
author = "Petrović, S. and Velickovic, N. and Stanojević, Ivana and Milošević, Maja and Drakulić, Dunja R. and Stanojlović, Miloš R. and Horvat, Anica",
year = "2011",
abstract = "Our results, as well as those of others, have indicated that 17 beta-estradiol (E2) exerts its nongenomic effects in neuronal cells by affecting plasma membrane Ca2+ flux. In neuronal cells mitochondria possess Ca2+ buffering properties as they both sequester and release Ca2+. The goal of this study was to examine the rapid non-genomic effect of E2 on mitochondria! Ca2+ transport in hippocampal synaptosomes from ovariectomised rats. In addition, we aimed to determine if, and to what extent, E2 receptors participated in mitochondria! Ca2+ transport modulation by E2 in vitro. E2-specific binding and Ca2+ transport was monitored. At physiological E2 concentrations (0.1-1.5 nmol/L), specific E2 binding to mitochondria isolated from hippocampal synaptosomes was detected with a B-max and K-m of 37.6 +/- 2.6 fmol/mg protein and 0.69 +/- 0.14 nmol/L of free E2, respectively. The main mitochondrial Ca2+ influx mechanism is the Ruthenium Red-sensitive uniporter driven by mitochondrial membrane potential. Despite no effect of E2 on Ca2+ influx, a physiological E2 concentration (0.5 nmol/L) protected mitochondrial membrane potential and consequently Ca2+ influx from the uncoupling agent carbonyl cyanide 4-(trifluoromethoxy)phenylhydrazone (1 mu mol/L). In neuronal cells the predominant mitochondria! Ca2+ efflux mechanism is the Na+/Ca2+ exchanger. E2 caused Ca2+ efflux inhibition (by 46%) coupled with increased affinity of the Na+/Ca2+ exchanger for Na+. Using E2 receptor (ER alpha and ER beta) antagonists and agonists, we confirmed ER betas involvement in E2-induced mitochondrial membrane potential protection as well as Ca2+ efflux inhibition. In summary, our results indicate that the nongenomic neuromodulatory role of E2 in rat hippocampus is achieved by affecting mitochondria! Ca2+ transport via, in part, mitochondrial ER beta. (C) 2011 IBRO. Published by Elsevier Ltd. All rights reserved.",
journal = "Neuroscience",
title = "Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus",
volume = "192",
pages = "195-204",
doi = "10.1016/j.neuroscience.2011.06.030"
}

Petrović, S., Velickovic, N., Stanojević, I., Milošević, M., Drakulić, D. R., Stanojlović, M. R.,& Horvat, A.. (2011). Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus. in Neuroscience, 192, 195-204.
https://doi.org/10.1016/j.neuroscience.2011.06.030

Petrović S, Velickovic N, Stanojević I, Milošević M, Drakulić DR, Stanojlović MR, Horvat A. Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus. in Neuroscience. 2011;192:195-204.
doi:10.1016/j.neuroscience.2011.06.030 .

Petrović, S., Velickovic, N., Stanojević, Ivana, Milošević, Maja, Drakulić, Dunja R., Stanojlović, Miloš R., Horvat, Anica, "Inhibition of Mitochondrial Na+-Dependent Ca2+ Efflux By 17 Beta-Estradiol in the Rat Hippocampus" in Neuroscience, 192 (2011):195-204,
https://doi.org/10.1016/j.neuroscience.2011.06.030 . .