TY  - JOUR
AU  - Jeremić, Rada
AU  - Peković, Sanja
AU  - Lavrnja, Irena
AU  - Bjelobaba, Ivana
AU  - Đelić, Marina
AU  - Dacić, Sanja
AU  - Brkić, Predrag D
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5975
AB  - A growing body of evidence suggests that hyperbaric oxygenation (HBO) may affect the activity of adult neural stem cells (NSCs). Since the role of NSCs in recovery from brain injury is still unclear, the purpose of this study was to investigate the effects of sensorimotor cortex ablation (SCA) and HBO treatment (HBOT) on the processes of neurogenesis in the adult dentate gyrus (DG), a region of the hippocampus that is the site of adult neurogenesis. Ten-week-old Wistar rats were divided into groups: Control (C, intact animals), Sham control (S, animals that underwent the surgical procedure without opening the skull), SCA (animals in whom the right sensorimotor cortex was removed via suction ablation), and SCA + HBO (operated animals that passed HBOT). HBOT protocol: pressure applied at 2.5 absolute atmospheres for 60 min, once daily for 10 days. Using immunohistochemistry and double immunofluorescence labeling, we show that SCA causes significant loss of neurons in the DG. Newborn neurons in the subgranular zone (SGZ), inner-third, and partially mid-third of the granule cell layer are predominantly affected by SCA. HBOT decreases the SCA-caused loss of immature neurons, prevents reduction of dendritic arborization, and increases proliferation of progenitor cells. Our results suggest a protective effect of HBO by reducing the vulnerability of immature neurons in the adult DG to SCA injury.
PB  - Basel: MDPI
T2  - International Journal of Molecular Sciences
T1  - Hyperbaric Oxygenation Prevents Loss of Immature Neurons in the Adult Hippocampal Dentate Gyrus Following Brain Injury
IS  - 5
VL  - 24
DO  - 10.3390/ijms24054261
SP  - 4261
ER  - 

@article{
author = "Jeremić, Rada and Peković, Sanja and Lavrnja, Irena and Bjelobaba, Ivana and Đelić, Marina and Dacić, Sanja and Brkić, Predrag D",
year = "2023",
abstract = "A growing body of evidence suggests that hyperbaric oxygenation (HBO) may affect the activity of adult neural stem cells (NSCs). Since the role of NSCs in recovery from brain injury is still unclear, the purpose of this study was to investigate the effects of sensorimotor cortex ablation (SCA) and HBO treatment (HBOT) on the processes of neurogenesis in the adult dentate gyrus (DG), a region of the hippocampus that is the site of adult neurogenesis. Ten-week-old Wistar rats were divided into groups: Control (C, intact animals), Sham control (S, animals that underwent the surgical procedure without opening the skull), SCA (animals in whom the right sensorimotor cortex was removed via suction ablation), and SCA + HBO (operated animals that passed HBOT). HBOT protocol: pressure applied at 2.5 absolute atmospheres for 60 min, once daily for 10 days. Using immunohistochemistry and double immunofluorescence labeling, we show that SCA causes significant loss of neurons in the DG. Newborn neurons in the subgranular zone (SGZ), inner-third, and partially mid-third of the granule cell layer are predominantly affected by SCA. HBOT decreases the SCA-caused loss of immature neurons, prevents reduction of dendritic arborization, and increases proliferation of progenitor cells. Our results suggest a protective effect of HBO by reducing the vulnerability of immature neurons in the adult DG to SCA injury.",
publisher = "Basel: MDPI",
journal = "International Journal of Molecular Sciences",
title = "Hyperbaric Oxygenation Prevents Loss of Immature Neurons in the Adult Hippocampal Dentate Gyrus Following Brain Injury",
number = "5",
volume = "24",
doi = "10.3390/ijms24054261",
pages = "4261"
}

Jeremić, R., Peković, S., Lavrnja, I., Bjelobaba, I., Đelić, M., Dacić, S.,& Brkić, P. D.. (2023). Hyperbaric Oxygenation Prevents Loss of Immature Neurons in the Adult Hippocampal Dentate Gyrus Following Brain Injury. in International Journal of Molecular Sciences
Basel: MDPI., 24(5), 4261.
https://doi.org/10.3390/ijms24054261

Jeremić R, Peković S, Lavrnja I, Bjelobaba I, Đelić M, Dacić S, Brkić PD. Hyperbaric Oxygenation Prevents Loss of Immature Neurons in the Adult Hippocampal Dentate Gyrus Following Brain Injury. in International Journal of Molecular Sciences. 2023;24(5):4261.
doi:10.3390/ijms24054261 .

Jeremić, Rada, Peković, Sanja, Lavrnja, Irena, Bjelobaba, Ivana, Đelić, Marina, Dacić, Sanja, Brkić, Predrag D, "Hyperbaric Oxygenation Prevents Loss of Immature Neurons in the Adult Hippocampal Dentate Gyrus Following Brain Injury" in International Journal of Molecular Sciences, 24, no. 5 (2023):4261,
https://doi.org/10.3390/ijms24054261 . .

TY  - CONF
AU  - Jeremić, Rada
AU  - Peković, Sanja
AU  - Lavrnja, Irena
AU  - Bjelobaba, Ivana
AU  - Đelić, Marina N
AU  - Brkić, Predrag D
AU  - Dacić, Sanja
PY  - 2023
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5984
AB  - Introduction: There is growing evidence that hyperbaric oxygenation (HBO) can affect adult neural stem cells (NSCs) activity. Because the role of NSCs in recovery from brain injury is still unclear, this study examined how ablation of the sensorimotor cortex (SCA) and HBO treatment (HBOT) affect the process of neurogenesis in the adult dentate gyrus (DG), a region of the hippocampus considered to be the site of adult neurogenesis. Material and methods: Ten-week-old Wistar rats were divided into groups: Control (C, intact animals), SCA (animals in which the right sensorimotor cortex was removed by suction ablation), and SCA+HBO (operated animals subjected to HBOT). HBOT protocol: pressure applied at 2.5 absolute atmospheres for 60 min, once daily for 10 days. The effects of HBOT were monitored by immunohistochemistry and double immunofluorescence labeling. In addition, the number of DCX+ cells was determined along the length of the SGZ in the inner and separately in the outer blade of the right dentate gyrus. Also, the total dendrite length was measured and the number of branching points, dendrite terminals, and segments were counted to quantify dendritic arborization in each neuron. Results: HBOT decreases SCA-induced loss of immature neurons, prevents reduction of dendritic branching, and increases proliferation of progenitor cells. Conclusion: Our results suggest a protective effect of HBOT by reducing the vulnerability of immature neurons in the adult DG to SCA injury.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia
T1  - Hyperbaric oxygen prevents dendrite degeneration and loss of DCX-positive newborn immature neurons in the dentate gyrus after traumatic brain injury
SP  - 78
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5984
ER  - 

@conference{
author = "Jeremić, Rada and Peković, Sanja and Lavrnja, Irena and Bjelobaba, Ivana and Đelić, Marina N and Brkić, Predrag D and Dacić, Sanja",
year = "2023",
abstract = "Introduction: There is growing evidence that hyperbaric oxygenation (HBO) can affect adult neural stem cells (NSCs) activity. Because the role of NSCs in recovery from brain injury is still unclear, this study examined how ablation of the sensorimotor cortex (SCA) and HBO treatment (HBOT) affect the process of neurogenesis in the adult dentate gyrus (DG), a region of the hippocampus considered to be the site of adult neurogenesis. Material and methods: Ten-week-old Wistar rats were divided into groups: Control (C, intact animals), SCA (animals in which the right sensorimotor cortex was removed by suction ablation), and SCA+HBO (operated animals subjected to HBOT). HBOT protocol: pressure applied at 2.5 absolute atmospheres for 60 min, once daily for 10 days. The effects of HBOT were monitored by immunohistochemistry and double immunofluorescence labeling. In addition, the number of DCX+ cells was determined along the length of the SGZ in the inner and separately in the outer blade of the right dentate gyrus. Also, the total dendrite length was measured and the number of branching points, dendrite terminals, and segments were counted to quantify dendritic arborization in each neuron. Results: HBOT decreases SCA-induced loss of immature neurons, prevents reduction of dendritic branching, and increases proliferation of progenitor cells. Conclusion: Our results suggest a protective effect of HBOT by reducing the vulnerability of immature neurons in the adult DG to SCA injury.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia",
title = "Hyperbaric oxygen prevents dendrite degeneration and loss of DCX-positive newborn immature neurons in the dentate gyrus after traumatic brain injury",
pages = "78",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5984"
}

Jeremić, R., Peković, S., Lavrnja, I., Bjelobaba, I., Đelić, M. N., Brkić, P. D.,& Dacić, S.. (2023). Hyperbaric oxygen prevents dendrite degeneration and loss of DCX-positive newborn immature neurons in the dentate gyrus after traumatic brain injury. in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 78.
https://hdl.handle.net/21.15107/rcub_ibiss_5984

Jeremić R, Peković S, Lavrnja I, Bjelobaba I, Đelić MN, Brkić PD, Dacić S. Hyperbaric oxygen prevents dendrite degeneration and loss of DCX-positive newborn immature neurons in the dentate gyrus after traumatic brain injury. in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia. 2023;:78.
https://hdl.handle.net/21.15107/rcub_ibiss_5984 .

Jeremić, Rada, Peković, Sanja, Lavrnja, Irena, Bjelobaba, Ivana, Đelić, Marina N, Brkić, Predrag D, Dacić, Sanja, "Hyperbaric oxygen prevents dendrite degeneration and loss of DCX-positive newborn immature neurons in the dentate gyrus after traumatic brain injury" in Book of abstracts: 8th Congress of Serbian neuroscience society with international participation; 2023 May 31 - Jun 2; Belgrade, Serbia (2023):78,
https://hdl.handle.net/21.15107/rcub_ibiss_5984 .

TY  - JOUR
AU  - Ćupić Miladinović, Dejana
AU  - Prevendar Crnić, Andreja
AU  - Peković, Sanja
AU  - Dacić, Sanja
AU  - Ivanović, Saša
AU  - Santibanez, Juan Francisco
AU  - Ćupić, Vitomir
AU  - Borozan, Nevena
AU  - Antonijević Miljaković, Evica
AU  - Borozan, Sunčica
PY  - 2020
UR  - https://linkinghub.elsevier.com/retrieve/pii/S0009279720315908
UR  - http://www.ncbi.nlm.nih.gov/pubmed/33166511
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4007
AB  - Chlorpyrifos is a extensively used organophosphate pesticide (OP). In this study, we closely looked into neurotoxicity of CPF and effect of vitamin B1, by checking the levels of cholinesterases, determining the activity of parameters of oxidative stress, inflammation and also level of apoptotic regulator. The study was performed on a total of 80 male Japanese quails (Coturnix japonica), (two control and 6 experimental groups, n = 10). Three group of quails were given by gavage chlorpyrifos (CPF) for 7 consecutive days at doses of 1.50 mg/kg b.w., 3.00 mg/kg b.w., and 6.00 mg/kg b.w. Another three groups were treated with 10 mg/kg b.w. of vitamin B1 i.m. 30 min after CPF application (in above mentioned doses). Our study have proved that all doses of CPF significantly inhibited cholinesterases in brain, while vitamin B1 reactivated them. CPF has led to an increase in the concentration of malondialdehyde (MDA), and activity of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), while tiamin changed the activity of antioxidant enzymes: CAT, SOD, GST. CPF stimulated apoptosis by decreasing B-cell lymphoma (Bcl-2) in brain, while application of vitamin B1 caused an increase of this parameter. CPF amplified inflammatory effect by elevating levels of inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX-2). Thiamine proved its anti-inflammatory property by decreasing the expression of iNOS and interleukin-1(IL-1) and interleukin-6(IL-6). This study is highly pertinent because there is little defense currently available to humans and animals to prevent toxic effects of pesticides.
PB  - Elsevier BV
T2  - Chemico-Biological Interactions
T1  - Recovery of brain cholinesterases and effect on parameters of oxidative stres and apoptosis in quails (Coturnix japonica) after chlorpyrifos and vitamin B1 administration.
DO  - 10.1016/j.cbi.2020.109312
SP  - 109312
ER  - 

@article{
author = "Ćupić Miladinović, Dejana and Prevendar Crnić, Andreja and Peković, Sanja and Dacić, Sanja and Ivanović, Saša and Santibanez, Juan Francisco and Ćupić, Vitomir and Borozan, Nevena and Antonijević Miljaković, Evica and Borozan, Sunčica",
year = "2020",
abstract = "Chlorpyrifos is a extensively used organophosphate pesticide (OP). In this study, we closely looked into neurotoxicity of CPF and effect of vitamin B1, by checking the levels of cholinesterases, determining the activity of parameters of oxidative stress, inflammation and also level of apoptotic regulator. The study was performed on a total of 80 male Japanese quails (Coturnix japonica), (two control and 6 experimental groups, n = 10). Three group of quails were given by gavage chlorpyrifos (CPF) for 7 consecutive days at doses of 1.50 mg/kg b.w., 3.00 mg/kg b.w., and 6.00 mg/kg b.w. Another three groups were treated with 10 mg/kg b.w. of vitamin B1 i.m. 30 min after CPF application (in above mentioned doses). Our study have proved that all doses of CPF significantly inhibited cholinesterases in brain, while vitamin B1 reactivated them. CPF has led to an increase in the concentration of malondialdehyde (MDA), and activity of catalase (CAT), superoxide dismutase (SOD), glutathione-S-transferase (GST), while tiamin changed the activity of antioxidant enzymes: CAT, SOD, GST. CPF stimulated apoptosis by decreasing B-cell lymphoma (Bcl-2) in brain, while application of vitamin B1 caused an increase of this parameter. CPF amplified inflammatory effect by elevating levels of inducible nitric oxide synthase (iNOS), and cyclooxygenase (COX-2). Thiamine proved its anti-inflammatory property by decreasing the expression of iNOS and interleukin-1(IL-1) and interleukin-6(IL-6). This study is highly pertinent because there is little defense currently available to humans and animals to prevent toxic effects of pesticides.",
publisher = "Elsevier BV",
journal = "Chemico-Biological Interactions",
title = "Recovery of brain cholinesterases and effect on parameters of oxidative stres and apoptosis in quails (Coturnix japonica) after chlorpyrifos and vitamin B1 administration.",
doi = "10.1016/j.cbi.2020.109312",
pages = "109312"
}

Ćupić Miladinović, D., Prevendar Crnić, A., Peković, S., Dacić, S., Ivanović, S., Santibanez, J. F., Ćupić, V., Borozan, N., Antonijević Miljaković, E.,& Borozan, S.. (2020). Recovery of brain cholinesterases and effect on parameters of oxidative stres and apoptosis in quails (Coturnix japonica) after chlorpyrifos and vitamin B1 administration.. in Chemico-Biological Interactions
Elsevier BV., 109312.
https://doi.org/10.1016/j.cbi.2020.109312

Ćupić Miladinović D, Prevendar Crnić A, Peković S, Dacić S, Ivanović S, Santibanez JF, Ćupić V, Borozan N, Antonijević Miljaković E, Borozan S. Recovery of brain cholinesterases and effect on parameters of oxidative stres and apoptosis in quails (Coturnix japonica) after chlorpyrifos and vitamin B1 administration.. in Chemico-Biological Interactions. 2020;:109312.
doi:10.1016/j.cbi.2020.109312 .

Ćupić Miladinović, Dejana, Prevendar Crnić, Andreja, Peković, Sanja, Dacić, Sanja, Ivanović, Saša, Santibanez, Juan Francisco, Ćupić, Vitomir, Borozan, Nevena, Antonijević Miljaković, Evica, Borozan, Sunčica, "Recovery of brain cholinesterases and effect on parameters of oxidative stres and apoptosis in quails (Coturnix japonica) after chlorpyrifos and vitamin B1 administration." in Chemico-Biological Interactions (2020):109312,
https://doi.org/10.1016/j.cbi.2020.109312 . .

TY  - JOUR
AU  - Ehmedah, Adil
AU  - Nedeljković, Predrag
AU  - Dacić, Sanja
AU  - Repac, Jelena
AU  - Drašković-Pavlović, Biljana
AU  - Vučević, Dragana
AU  - Peković, Sanja
AU  - Božić Nedeljković, Biljana
PY  - 2020
UR  - https://www.mdpi.com/1420-3049/25/22/5426
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/4034
AB  - Peripheral nerve injury (PNI) triggers a complex multi-cellular response involving the injured neurons, Schwann cells (SCs), and immune cells, often resulting in poor functional recovery. The aim of this study was to investigate the effects of the treatment with vitamin B (B1, B2, B3, B5, B6, and B12) complex on the interaction between macrophages and SCs during the recovery period after PNI. Transection of the motor branch of the femoral nerve followed by reconstruction by termino-terminal anastomosis was used as an experimental model. Isolated nerves from the sham (S), operated (O), and operated groups treated with the B vitamins (OT group) were used for immunofluorescence analysis. The obtained data indicated that PNI modulates interactions between macrophages and SCs in a time-dependent manner. The treatment with B vitamins complex promoted the M1-to M2-macrophage polarization and accelerated the transition from the non-myelin to myelin-forming SCs, an indicative of SCs maturation. The effect of B vitamins complex on both cell types was accompanied with an increase in macrophage/SC interactions, all of which correlated with the regeneration of the injured nerve. Clearly, the capacity of B vitamins to modulate macrophages-SCs interaction may be promising for the treatment of PNI.
PB  - NLM (Medline)
T2  - Molecules
T1  - Effect of Vitamin B Complex Treatment on Macrophages to Schwann Cells Association during Neuroinflammation after Peripheral Nerve Injury
IS  - 22
VL  - 25
DO  - 10.3390/molecules25225426
SP  - 5426
ER  - 

@article{
author = "Ehmedah, Adil and Nedeljković, Predrag and Dacić, Sanja and Repac, Jelena and Drašković-Pavlović, Biljana and Vučević, Dragana and Peković, Sanja and Božić Nedeljković, Biljana",
year = "2020",
abstract = "Peripheral nerve injury (PNI) triggers a complex multi-cellular response involving the injured neurons, Schwann cells (SCs), and immune cells, often resulting in poor functional recovery. The aim of this study was to investigate the effects of the treatment with vitamin B (B1, B2, B3, B5, B6, and B12) complex on the interaction between macrophages and SCs during the recovery period after PNI. Transection of the motor branch of the femoral nerve followed by reconstruction by termino-terminal anastomosis was used as an experimental model. Isolated nerves from the sham (S), operated (O), and operated groups treated with the B vitamins (OT group) were used for immunofluorescence analysis. The obtained data indicated that PNI modulates interactions between macrophages and SCs in a time-dependent manner. The treatment with B vitamins complex promoted the M1-to M2-macrophage polarization and accelerated the transition from the non-myelin to myelin-forming SCs, an indicative of SCs maturation. The effect of B vitamins complex on both cell types was accompanied with an increase in macrophage/SC interactions, all of which correlated with the regeneration of the injured nerve. Clearly, the capacity of B vitamins to modulate macrophages-SCs interaction may be promising for the treatment of PNI.",
publisher = "NLM (Medline)",
journal = "Molecules",
title = "Effect of Vitamin B Complex Treatment on Macrophages to Schwann Cells Association during Neuroinflammation after Peripheral Nerve Injury",
number = "22",
volume = "25",
doi = "10.3390/molecules25225426",
pages = "5426"
}

Ehmedah, A., Nedeljković, P., Dacić, S., Repac, J., Drašković-Pavlović, B., Vučević, D., Peković, S.,& Božić Nedeljković, B.. (2020). Effect of Vitamin B Complex Treatment on Macrophages to Schwann Cells Association during Neuroinflammation after Peripheral Nerve Injury. in Molecules
NLM (Medline)., 25(22), 5426.
https://doi.org/10.3390/molecules25225426

Ehmedah A, Nedeljković P, Dacić S, Repac J, Drašković-Pavlović B, Vučević D, Peković S, Božić Nedeljković B. Effect of Vitamin B Complex Treatment on Macrophages to Schwann Cells Association during Neuroinflammation after Peripheral Nerve Injury. in Molecules. 2020;25(22):5426.
doi:10.3390/molecules25225426 .

Ehmedah, Adil, Nedeljković, Predrag, Dacić, Sanja, Repac, Jelena, Drašković-Pavlović, Biljana, Vučević, Dragana, Peković, Sanja, Božić Nedeljković, Biljana, "Effect of Vitamin B Complex Treatment on Macrophages to Schwann Cells Association during Neuroinflammation after Peripheral Nerve Injury" in Molecules, 25, no. 22 (2020):5426,
https://doi.org/10.3390/molecules25225426 . .

TY  - JOUR
AU  - Pantić, Igor
AU  - Jeremić, Rada
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Pantić, Senka
AU  - Đelić, Marina
AU  - Vitić, Zagorka
AU  - Brkić, Predrag
AU  - Brodski, Claude
PY  - 2020
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3599
AB  - Traumatic brain injury (TBI) is a main cause of death and disabilities in young adults. Although learning and memory impairments are a major clinical manifestation of TBI, the consequences of TBI on the hippocampus are still not well understood. In particular, how lesions to the sensorimotor cortex damage the hippocampus, to which it is not directly connected, is still elusive. Here, we study the effects of sensorimotor cortex ablation (SCA) on the hippocampal dentate gyrus, by applying a highly sensitive gray-level co-occurrence matrix (GLCM) analysis. Using GLCM analysis of granule neurons, we discovered, in our TBI paradigm, subtle changes in granule cell (GC) morphology, including textual uniformity, contrast, and variance, which is not detected by conventional microscopy. We conclude that sensorimotor cortex trauma leads to specific changes in the hippocampus that advance our understanding of the cellular underpinnings of cognitive impairments in TBI. Moreover, we identified GLCM analysis as a highly sensitive method to detect subtle changes in the GC layers that is expected to significantly improve further studies investigating the impact of TBI on hippocampal neuropathology.
T2  - Microscopy and Microanalysis
T1  - Gray-Level Co-Occurrence Matrix Analysis of Granule Neurons of the Hippocampal Dentate Gyrus Following Cortical Injury.
IS  - 1
VL  - 26
DO  - 10.1017/S143192762000001X
SP  - 166
EP  - 172
ER  - 

@article{
author = "Pantić, Igor and Jeremić, Rada and Dacić, Sanja and Peković, Sanja and Pantić, Senka and Đelić, Marina and Vitić, Zagorka and Brkić, Predrag and Brodski, Claude",
year = "2020",
abstract = "Traumatic brain injury (TBI) is a main cause of death and disabilities in young adults. Although learning and memory impairments are a major clinical manifestation of TBI, the consequences of TBI on the hippocampus are still not well understood. In particular, how lesions to the sensorimotor cortex damage the hippocampus, to which it is not directly connected, is still elusive. Here, we study the effects of sensorimotor cortex ablation (SCA) on the hippocampal dentate gyrus, by applying a highly sensitive gray-level co-occurrence matrix (GLCM) analysis. Using GLCM analysis of granule neurons, we discovered, in our TBI paradigm, subtle changes in granule cell (GC) morphology, including textual uniformity, contrast, and variance, which is not detected by conventional microscopy. We conclude that sensorimotor cortex trauma leads to specific changes in the hippocampus that advance our understanding of the cellular underpinnings of cognitive impairments in TBI. Moreover, we identified GLCM analysis as a highly sensitive method to detect subtle changes in the GC layers that is expected to significantly improve further studies investigating the impact of TBI on hippocampal neuropathology.",
journal = "Microscopy and Microanalysis",
title = "Gray-Level Co-Occurrence Matrix Analysis of Granule Neurons of the Hippocampal Dentate Gyrus Following Cortical Injury.",
number = "1",
volume = "26",
doi = "10.1017/S143192762000001X",
pages = "166-172"
}

Pantić, I., Jeremić, R., Dacić, S., Peković, S., Pantić, S., Đelić, M., Vitić, Z., Brkić, P.,& Brodski, C.. (2020). Gray-Level Co-Occurrence Matrix Analysis of Granule Neurons of the Hippocampal Dentate Gyrus Following Cortical Injury.. in Microscopy and Microanalysis, 26(1), 166-172.
https://doi.org/10.1017/S143192762000001X

Pantić I, Jeremić R, Dacić S, Peković S, Pantić S, Đelić M, Vitić Z, Brkić P, Brodski C. Gray-Level Co-Occurrence Matrix Analysis of Granule Neurons of the Hippocampal Dentate Gyrus Following Cortical Injury.. in Microscopy and Microanalysis. 2020;26(1):166-172.
doi:10.1017/S143192762000001X .

Pantić, Igor, Jeremić, Rada, Dacić, Sanja, Peković, Sanja, Pantić, Senka, Đelić, Marina, Vitić, Zagorka, Brkić, Predrag, Brodski, Claude, "Gray-Level Co-Occurrence Matrix Analysis of Granule Neurons of the Hippocampal Dentate Gyrus Following Cortical Injury." in Microscopy and Microanalysis, 26, no. 1 (2020):166-172,
https://doi.org/10.1017/S143192762000001X . .

TY  - JOUR
AU  - Dacić, Sanja
AU  - Božić, Iva
AU  - Jeremić, Rada
AU  - Bjelobaba, Ivana
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
AU  - Peković, Sanja
PY  - 2019
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5989
AB  - Aims: Traumatic brain injury (TBI) causes disruption in homeostasis of calcium ions (Ca2+), important second messenger considered as the major culprit of secondary injury and TBI-induced neuronal damage and death. Ca2+ entry into the cells occurs via various types of voltage-dependent calcium channels (VDCCs). The aim of this study was to evaluate the involvement of Ca2+ entry via L-type CaV1.2 VDCCs in the processes of neuroinflammation and regeneration after brain injury. Methods: TBI was performed on male Wistar rats by sensorimotor cortex ablation (SCA) at the following coordinates: 2 mm anterior and 4 mm posterior to bregma, and 4 mm lateral from the midline. Temporal and cellular pattern of CaV1.2 expression was followed at different time points post-injury (2, 7, 14, 30 dpi) using double immunofluorescence staining with specific markers. Results: Upregulation of CaV1.2 expression was detected on reactive astrocytes and astrocytic processes that form glial scar around the lesion site, on subset of proinflammatory microglia/macrophages and neutrophils surrounding the lesion cavity. Interestingly, presence of CaV1.2+ cells was detected in the migratory pathway, consisted of DCX+ progenitors, extending from subventricular zone up to the lesion site. Furthermore, CaV1.2+/DCX+ newborn neurons were detected in subgranular layer of hippocampal dentate gyrus. Conclusions: We concluded that L-type CaV1.2 calcium channel has an important role in the regulation of processes of neuroinflammation, neuroregeneration and neurogenesis, pointing to the complexity of intercellular regulation of Ca2+ homeostasis after brain injury. Consequently, modulation of CaV1.2 channels expression may be potential target for the treatment of brain injury.
PB  - Belgrade: Serbian Neuroscience Society
T2  - Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
T1  - L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury
SP  - 487
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5989
ER  - 

@article{
author = "Dacić, Sanja and Božić, Iva and Jeremić, Rada and Bjelobaba, Ivana and Lavrnja, Irena and Savić, Danijela and Rakić, Ljubisav and Stojiljković, Mirjana and Peković, Sanja",
year = "2019",
abstract = "Aims: Traumatic brain injury (TBI) causes disruption in homeostasis of calcium ions (Ca2+), important second messenger considered as the major culprit of secondary injury and TBI-induced neuronal damage and death. Ca2+ entry into the cells occurs via various types of voltage-dependent calcium channels (VDCCs). The aim of this study was to evaluate the involvement of Ca2+ entry via L-type CaV1.2 VDCCs in the processes of neuroinflammation and regeneration after brain injury. Methods: TBI was performed on male Wistar rats by sensorimotor cortex ablation (SCA) at the following coordinates: 2 mm anterior and 4 mm posterior to bregma, and 4 mm lateral from the midline. Temporal and cellular pattern of CaV1.2 expression was followed at different time points post-injury (2, 7, 14, 30 dpi) using double immunofluorescence staining with specific markers. Results: Upregulation of CaV1.2 expression was detected on reactive astrocytes and astrocytic processes that form glial scar around the lesion site, on subset of proinflammatory microglia/macrophages and neutrophils surrounding the lesion cavity. Interestingly, presence of CaV1.2+ cells was detected in the migratory pathway, consisted of DCX+ progenitors, extending from subventricular zone up to the lesion site. Furthermore, CaV1.2+/DCX+ newborn neurons were detected in subgranular layer of hippocampal dentate gyrus. Conclusions: We concluded that L-type CaV1.2 calcium channel has an important role in the regulation of processes of neuroinflammation, neuroregeneration and neurogenesis, pointing to the complexity of intercellular regulation of Ca2+ homeostasis after brain injury. Consequently, modulation of CaV1.2 channels expression may be potential target for the treatment of brain injury.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia",
title = "L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury",
pages = "487",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5989"
}

Dacić, S., Božić, I., Jeremić, R., Bjelobaba, I., Lavrnja, I., Savić, D., Rakić, L., Stojiljković, M.,& Peković, S.. (2019). L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 487.
https://hdl.handle.net/21.15107/rcub_ibiss_5989

Dacić S, Božić I, Jeremić R, Bjelobaba I, Lavrnja I, Savić D, Rakić L, Stojiljković M, Peković S. L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury. in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. 2019;:487.
https://hdl.handle.net/21.15107/rcub_ibiss_5989 .

Dacić, Sanja, Božić, Iva, Jeremić, Rada, Bjelobaba, Ivana, Lavrnja, Irena, Savić, Danijela, Rakić, Ljubisav, Stojiljković, Mirjana, Peković, Sanja, "L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury" in Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia (2019):487,
https://hdl.handle.net/21.15107/rcub_ibiss_5989 .

TY  - CONF
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Bjelobaba, Ivana
AU  - Dacić, Sanja
AU  - Laketa, Danijela
AU  - Božić, Iva
AU  - Jakovljević, Marija
AU  - Nedeljković, Nadežda
AU  - Rakić, Ljubisav
AU  - Peković, Sanja
PY  - 2018
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5888
AB  - Ribavirin je purinski nukleozidni analog, otkriven pre više decenija i odobren kao lek protiv virusa hepatitisa C. Sa otkrićem direktnih antivirusnih agenasa, nastupila je revolucija u lečenju hepatitisa C, a terapijska uloga ribavirina je marginalizovana. Međutim, ribavirin ima širok spektar dejstva što je otvorilo mogućnost da se ovaj lek preusmeri ka tretmanu drugih oboljenja. Naime, osim što deluje antivirusno (inhibicija virusne RNK polimeraze i izazivanje letalne mutageneze) ribavirin je i inhibitor eukariotskog faktora za inicijaciju translacije e4E, što je zaslužno za njegov anti-tumorski efekat, pokazan u leukemiji i na ćelijama glioma. Njegova druga opšte poznata unutarćelijska meta jeste enzim inozin-5’-monofosfat dehidrogenaza (IMPDH), koji predstavlja ključni faktor u de novo sintezi guaninskih nukleotida. Ćelije koje se isključivo na ovaj način snabdevaju purinskim nukleotidima, kao što su aktivirani limfociti i neke proliferišuće ćelije, izuzetno su senzitivne na delovanje ribavirina. Inhibicija IMPDH odgovorna je za imunosupresivno i imunomodulatorno dejstvo ribavirina, pokazano u in vitro i in vivo modelima neuroinflamacije. Dakle, iako ribavirin gubi centralnu ulogu koju je imao u terapiji infekcije virusom hepatitisa C, njegova multipotentna priroda koja se ogleda u različitim mehanizmima delovanja, predstavlja potencijal za preusmeravanje ka novim terapijskim indikacijama, kao što su kancer ili multipla skleroza.
PB  - Belgrade: Serbian Biological Society
C3  - Drugi kongres biologa Srbije; 2018 Sep 25-30; Kladovo, Srbija
T1  - Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija
SP  - 146
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5888
ER  - 

@conference{
author = "Savić, Danijela and Lavrnja, Irena and Bjelobaba, Ivana and Dacić, Sanja and Laketa, Danijela and Božić, Iva and Jakovljević, Marija and Nedeljković, Nadežda and Rakić, Ljubisav and Peković, Sanja",
year = "2018",
abstract = "Ribavirin je purinski nukleozidni analog, otkriven pre više decenija i odobren kao lek protiv virusa hepatitisa C. Sa otkrićem direktnih antivirusnih agenasa, nastupila je revolucija u lečenju hepatitisa C, a terapijska uloga ribavirina je marginalizovana. Međutim, ribavirin ima širok spektar dejstva što je otvorilo mogućnost da se ovaj lek preusmeri ka tretmanu drugih oboljenja. Naime, osim što deluje antivirusno (inhibicija virusne RNK polimeraze i izazivanje letalne mutageneze) ribavirin je i inhibitor eukariotskog faktora za inicijaciju translacije e4E, što je zaslužno za njegov anti-tumorski efekat, pokazan u leukemiji i na ćelijama glioma. Njegova druga opšte poznata unutarćelijska meta jeste enzim inozin-5’-monofosfat dehidrogenaza (IMPDH), koji predstavlja ključni faktor u de novo sintezi guaninskih nukleotida. Ćelije koje se isključivo na ovaj način snabdevaju purinskim nukleotidima, kao što su aktivirani limfociti i neke proliferišuće ćelije, izuzetno su senzitivne na delovanje ribavirina. Inhibicija IMPDH odgovorna je za imunosupresivno i imunomodulatorno dejstvo ribavirina, pokazano u in vitro i in vivo modelima neuroinflamacije. Dakle, iako ribavirin gubi centralnu ulogu koju je imao u terapiji infekcije virusom hepatitisa C, njegova multipotentna priroda koja se ogleda u različitim mehanizmima delovanja, predstavlja potencijal za preusmeravanje ka novim terapijskim indikacijama, kao što su kancer ili multipla skleroza.",
publisher = "Belgrade: Serbian Biological Society",
journal = "Drugi kongres biologa Srbije; 2018 Sep 25-30; Kladovo, Srbija",
title = "Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija",
pages = "146",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5888"
}

Savić, D., Lavrnja, I., Bjelobaba, I., Dacić, S., Laketa, D., Božić, I., Jakovljević, M., Nedeljković, N., Rakić, L.,& Peković, S.. (2018). Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija. in Drugi kongres biologa Srbije; 2018 Sep 25-30; Kladovo, Srbija
Belgrade: Serbian Biological Society., 146.
https://hdl.handle.net/21.15107/rcub_ibiss_5888

Savić D, Lavrnja I, Bjelobaba I, Dacić S, Laketa D, Božić I, Jakovljević M, Nedeljković N, Rakić L, Peković S. Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija. in Drugi kongres biologa Srbije; 2018 Sep 25-30; Kladovo, Srbija. 2018;:146.
https://hdl.handle.net/21.15107/rcub_ibiss_5888 .

Savić, Danijela, Lavrnja, Irena, Bjelobaba, Ivana, Dacić, Sanja, Laketa, Danijela, Božić, Iva, Jakovljević, Marija, Nedeljković, Nadežda, Rakić, Ljubisav, Peković, Sanja, "Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija" in Drugi kongres biologa Srbije; 2018 Sep 25-30; Kladovo, Srbija (2018):146,
https://hdl.handle.net/21.15107/rcub_ibiss_5888 .

TY  - CONF
AU  - Laketa, Danijela
AU  - Josipović, Nataša
AU  - Lavrnja, Irena
AU  - Bjelobaba, Ivana
AU  - Jakovljević, Marija
AU  - Božić, Iva
AU  - Savić, Danijela
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Nedeljković, Nadežda
PY  - 2017
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5988
AB  - Introduction. Ecto-5'–nucleotidase (eN) catalyzes terminal step of extracellular ATP hydrolysis, producing anti-inflammatory adenosine. We reported significantly increased eN activity in lumbar spinal cord during experimental autoimmune encephalomyelitis (EAE), together with increased protein expression connected mainly with reactive astrocytes and appearance of new isoform at ~75kDa at the peak of the disease, besides usual ~71kDa isoform. Since eN is glycoprotein with five potential N-glycosylation sites and 
redicted molecular weight of 57-59 kDa, we hypothesized that occurrence of second isoform during EAE is due to changes in glycosylation pattern, possibly affecting kinetic properties of the enzyme. Methods. Lumbar parts of the spinal cords were obtained from Dark Agouti rats at the onset (Eo), peak (Ep) and the end of symptoms (Er) during EAE and from naïve control animals (C). Results. We here report significant changes of kinetic properties regarding AMP-hydrolysis during EAE, with almost 50% increase of maximal velocity at Ep (92.35±1.86nmolPi/min/mg) and Er (90.68±2.17nmolPi/min/mg), compared to C, whilst Km increased double at Ep (0.041±0.003mmol/l). Enzymatic deglycosylation caused triple decrease of Vmax (33.6±1.8nmolPi/mg/min) at Ep, and double decrease of Km (0.022±0.008mmol/l), whilst immunoblot
probed with anti-eN antibody revealed triple protein band at ~60kDa at all investigated time-points. Conclusion. Our results show that changes of kinetic properties during EAE, at least partially, are governed by modification of glycosylation pattern. Also, appearance of new isoform at the peak of EAE is direct consequence of glycosylation changes. In summary, besides gene and protein expression changes of eN, glycosylation might be additional route of inflammation control conducted by astrocytes.
PB  - Belgrade: Serbian Neuroscience Society
C3  - Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
T1  - Appearance of second ecto-5'-nucleotidase isoform during experimental autoimmune encephalomyelitis is caused by changes in glycosylation pattern
SP  - 70
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5988
ER  - 

@conference{
author = "Laketa, Danijela and Josipović, Nataša and Lavrnja, Irena and Bjelobaba, Ivana and Jakovljević, Marija and Božić, Iva and Savić, Danijela and Dacić, Sanja and Peković, Sanja and Nedeljković, Nadežda",
year = "2017",
abstract = "Introduction. Ecto-5'–nucleotidase (eN) catalyzes terminal step of extracellular ATP hydrolysis, producing anti-inflammatory adenosine. We reported significantly increased eN activity in lumbar spinal cord during experimental autoimmune encephalomyelitis (EAE), together with increased protein expression connected mainly with reactive astrocytes and appearance of new isoform at ~75kDa at the peak of the disease, besides usual ~71kDa isoform. Since eN is glycoprotein with five potential N-glycosylation sites and 
redicted molecular weight of 57-59 kDa, we hypothesized that occurrence of second isoform during EAE is due to changes in glycosylation pattern, possibly affecting kinetic properties of the enzyme. Methods. Lumbar parts of the spinal cords were obtained from Dark Agouti rats at the onset (Eo), peak (Ep) and the end of symptoms (Er) during EAE and from naïve control animals (C). Results. We here report significant changes of kinetic properties regarding AMP-hydrolysis during EAE, with almost 50% increase of maximal velocity at Ep (92.35±1.86nmolPi/min/mg) and Er (90.68±2.17nmolPi/min/mg), compared to C, whilst Km increased double at Ep (0.041±0.003mmol/l). Enzymatic deglycosylation caused triple decrease of Vmax (33.6±1.8nmolPi/mg/min) at Ep, and double decrease of Km (0.022±0.008mmol/l), whilst immunoblot
probed with anti-eN antibody revealed triple protein band at ~60kDa at all investigated time-points. Conclusion. Our results show that changes of kinetic properties during EAE, at least partially, are governed by modification of glycosylation pattern. Also, appearance of new isoform at the peak of EAE is direct consequence of glycosylation changes. In summary, besides gene and protein expression changes of eN, glycosylation might be additional route of inflammation control conducted by astrocytes.",
publisher = "Belgrade: Serbian Neuroscience Society",
journal = "Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia",
title = "Appearance of second ecto-5'-nucleotidase isoform during experimental autoimmune encephalomyelitis is caused by changes in glycosylation pattern",
pages = "70",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5988"
}

Laketa, D., Josipović, N., Lavrnja, I., Bjelobaba, I., Jakovljević, M., Božić, I., Savić, D., Dacić, S., Peković, S.,& Nedeljković, N.. (2017). Appearance of second ecto-5'-nucleotidase isoform during experimental autoimmune encephalomyelitis is caused by changes in glycosylation pattern. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia
Belgrade: Serbian Neuroscience Society., 70.
https://hdl.handle.net/21.15107/rcub_ibiss_5988

Laketa D, Josipović N, Lavrnja I, Bjelobaba I, Jakovljević M, Božić I, Savić D, Dacić S, Peković S, Nedeljković N. Appearance of second ecto-5'-nucleotidase isoform during experimental autoimmune encephalomyelitis is caused by changes in glycosylation pattern. in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia. 2017;:70.
https://hdl.handle.net/21.15107/rcub_ibiss_5988 .

Laketa, Danijela, Josipović, Nataša, Lavrnja, Irena, Bjelobaba, Ivana, Jakovljević, Marija, Božić, Iva, Savić, Danijela, Dacić, Sanja, Peković, Sanja, Nedeljković, Nadežda, "Appearance of second ecto-5'-nucleotidase isoform during experimental autoimmune encephalomyelitis is caused by changes in glycosylation pattern" in Book of Abstract: 7th Congress of Serbian Neuroscience Society with international participation; 2017 Oct 25-27; Belgrade, Serbia (2017):70,
https://hdl.handle.net/21.15107/rcub_ibiss_5988 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Parabucki, Ana
AU  - Bjelobaba, Ivana
AU  - Santrač, Anja
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
PY  - 2013
PY  - 2013
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/507
AB  - Background: Various in vivo and in vitro models have been described in order to elucidate the pathobiology underlying the traumatic brain injury (TBI) and test potentially suitable treatments. Since TBI is a complex disease, models differ in regard to the aspect of TBI that is being investigated. One of the used in vitro models is the scratch wound assay, first established as a reproducible, low-cost assay for the analysis of cell migration in vitro. The aim of the present study was to further investigate the relevancy of this model as a counter­part of in vivo TBI models. Methods: We have examined the astrocytic response to a mechanical injury in terms of expression of chondroitin sulfate proteoglycans (CSPGs) - phosphacan, neurocan and brevican, using real-time PCR and immunocytochemistry. Results: Our results indicate that in vitro scratch wounding alters the expression profile of examined CSPGs. Four hours after the scratch injury of the astrocytic monolayer, real-time PCR analysis revealed upregulation of mRNA levels for phosphacan (3-fold) and neurocan (2-fold), whereas brevican mRNA was downregulated (2-fold). Immunofluorescent signal for phosphacan and neurocan was more intense in astrocytes close to the injury site, while brevican was scarcely present in cultured astrocytes. Conclusions: Obtained results indicate that CSPGs are differentially expressed by astrocytes after scratch wounding, demonstrating that the scratch wound model might be suitable for investigation of astrocyte-derived response to injury.
AB  - Uvod: Brojni in vivo i in vitro modeli opisani su sa ciljem da se rasvetle patobiološki procesi koji su osnova traumatske povrede mozga (TPM) i testiraju potencijalni tretmani. Imajući u vidu da je TPM kompleksno oboljenje, ovi modeli se međusobno razlikuju shodno aspektu TPM koji se ispituje. Jedan od in vitro modela je i povreda ćelijskog jednosloja grebanjem (engl. 'scratch wound' assay), isprva ustanovljen kao ponovljiv, jeftin test za analizu celijske migracije in vitro. Cilj ove studije je da se bliže ispita relevantnost ovog modela u odnosu na in vivo modele TPM. Metode: Da bi se istražio odgovor astrocita na mehaničku povredu, praćena je ekspresija odabranih hondroitin-sulfatnih proteoglikana (CSPG) - fosfakana, neurokana i brevikana, korišćenjem PCR u realnom vremenu i imunocitohemije. Rezultati: Dobijeni rezultati su pokazali da in vitro povreda astrocitnog jednosloja menja profile ekspresije ispitivanih CSPG. Četiri sata nakon povrede, primena PCR u realnom vremenu analize pokazala je povećanje nivoa iRNK za fosfakan (trostruko) i neurokan (dvostruko), dok je iRNK za brevikan bila smanjena na polovinu kontrolne vrednosti. Imunofluorescentni signal poreklom od fosfakana i neurokana je bio intenzivniji u astrocitima bližim mestu povrede, dok je signal za brevikan bio slab kako u kontrolnoj, tako i u ozleđenoj grupi. Zaključak: Dobijeni rezultati pokazuju da povreda izazvana grebanjem različito utiče na ekspresiju ispitivanih CSPG u astrocitima, sto ukazuju da ovaj model može biti pogodan za ispitivanje odgovora astrocita na povredu.
T2  - Journal of Medical Biochemistry
T1  - PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi
T1  - Real-time PCR and immunocytochemical study of chondroitin sulfate proteoglycans after scratch wounding in cultured astrocytes
IS  - 4
VL  - 32
SP  - 398
EP  - 405
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_507
ER  - 

@article{
author = "Savić, Danijela and Parabucki, Ana and Bjelobaba, Ivana and Santrač, Anja and Dacić, Sanja and Peković, Sanja and Stojiljković, Mirjana",
year = "2013, 2013",
abstract = "Background: Various in vivo and in vitro models have been described in order to elucidate the pathobiology underlying the traumatic brain injury (TBI) and test potentially suitable treatments. Since TBI is a complex disease, models differ in regard to the aspect of TBI that is being investigated. One of the used in vitro models is the scratch wound assay, first established as a reproducible, low-cost assay for the analysis of cell migration in vitro. The aim of the present study was to further investigate the relevancy of this model as a counter­part of in vivo TBI models. Methods: We have examined the astrocytic response to a mechanical injury in terms of expression of chondroitin sulfate proteoglycans (CSPGs) - phosphacan, neurocan and brevican, using real-time PCR and immunocytochemistry. Results: Our results indicate that in vitro scratch wounding alters the expression profile of examined CSPGs. Four hours after the scratch injury of the astrocytic monolayer, real-time PCR analysis revealed upregulation of mRNA levels for phosphacan (3-fold) and neurocan (2-fold), whereas brevican mRNA was downregulated (2-fold). Immunofluorescent signal for phosphacan and neurocan was more intense in astrocytes close to the injury site, while brevican was scarcely present in cultured astrocytes. Conclusions: Obtained results indicate that CSPGs are differentially expressed by astrocytes after scratch wounding, demonstrating that the scratch wound model might be suitable for investigation of astrocyte-derived response to injury., Uvod: Brojni in vivo i in vitro modeli opisani su sa ciljem da se rasvetle patobiološki procesi koji su osnova traumatske povrede mozga (TPM) i testiraju potencijalni tretmani. Imajući u vidu da je TPM kompleksno oboljenje, ovi modeli se međusobno razlikuju shodno aspektu TPM koji se ispituje. Jedan od in vitro modela je i povreda ćelijskog jednosloja grebanjem (engl. 'scratch wound' assay), isprva ustanovljen kao ponovljiv, jeftin test za analizu celijske migracije in vitro. Cilj ove studije je da se bliže ispita relevantnost ovog modela u odnosu na in vivo modele TPM. Metode: Da bi se istražio odgovor astrocita na mehaničku povredu, praćena je ekspresija odabranih hondroitin-sulfatnih proteoglikana (CSPG) - fosfakana, neurokana i brevikana, korišćenjem PCR u realnom vremenu i imunocitohemije. Rezultati: Dobijeni rezultati su pokazali da in vitro povreda astrocitnog jednosloja menja profile ekspresije ispitivanih CSPG. Četiri sata nakon povrede, primena PCR u realnom vremenu analize pokazala je povećanje nivoa iRNK za fosfakan (trostruko) i neurokan (dvostruko), dok je iRNK za brevikan bila smanjena na polovinu kontrolne vrednosti. Imunofluorescentni signal poreklom od fosfakana i neurokana je bio intenzivniji u astrocitima bližim mestu povrede, dok je signal za brevikan bio slab kako u kontrolnoj, tako i u ozleđenoj grupi. Zaključak: Dobijeni rezultati pokazuju da povreda izazvana grebanjem različito utiče na ekspresiju ispitivanih CSPG u astrocitima, sto ukazuju da ovaj model može biti pogodan za ispitivanje odgovora astrocita na povredu.",
journal = "Journal of Medical Biochemistry",
title = "PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi, Real-time PCR and immunocytochemical study of chondroitin sulfate proteoglycans after scratch wounding in cultured astrocytes",
number = "4",
volume = "32",
pages = "398-405",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_507"
}

Savić, D., Parabucki, A., Bjelobaba, I., Santrač, A., Dacić, S., Peković, S.,& Stojiljković, M.. (2013). PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi. in Journal of Medical Biochemistry, 32(4), 398-405.
https://hdl.handle.net/21.15107/rcub_ibiss_507

Savić D, Parabucki A, Bjelobaba I, Santrač A, Dacić S, Peković S, Stojiljković M. PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi. in Journal of Medical Biochemistry. 2013;32(4):398-405.
https://hdl.handle.net/21.15107/rcub_ibiss_507 .

Savić, Danijela, Parabucki, Ana, Bjelobaba, Ivana, Santrač, Anja, Dacić, Sanja, Peković, Sanja, Stojiljković, Mirjana, "PCR i imunocitohemijska studija ekspresije hondroitin-sulfatnih proteoglikana nakon povrede astrocita u kulturi" in Journal of Medical Biochemistry, 32, no. 4 (2013):398-405,
https://hdl.handle.net/21.15107/rcub_ibiss_507 .

TY  - JOUR
AU  - Savić, Danijela
AU  - Lavrnja, Irena
AU  - Dacić, Sanja
AU  - Bjelobaba, Ivana
AU  - Nedeljković, Nadežda
AU  - Peković, Sanja
AU  - Stojiljković, Mirjana
PY  - 2012
PY  - 2012
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/317
AB  - Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a human inflammatory and demyelinating disease. Microglia and astrocytes are glial cells of the central nervous system (CNS) that play a dual role in MS and EAE pathology. The aim of this study was to examine the effect of combined treatment with two nucleoside analogues, ribavirin and tiazofurin, on microglia and astrocytes in actively induced EAE. Therapeutic treatment with a combination of these two nucleoside analogues reduced disease severity, mononuclear cell infiltration and demyelination. The obtained histological results indicate that ribavirin and tiazofurin changed activated microglia into an inactive type and attenuated astrocyte reactivity at the end of the treatment period. Since reduction of reactive microgliosis and astrogliosis correlated with EAE suppression, the present study also suggests that the obtained beneficial effect of ribavirin and tiazofurin could be a consequence of their action inside as well as outside the CNS.
T2  - Archives of Biological Sciences
T1  - Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis
IS  - 3
VL  - 64
SP  - 843
EP  - 850
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_317
ER  - 

@article{
author = "Savić, Danijela and Lavrnja, Irena and Dacić, Sanja and Bjelobaba, Ivana and Nedeljković, Nadežda and Peković, Sanja and Stojiljković, Mirjana",
year = "2012, 2012",
abstract = "Experimental autoimmune encephalomyelitis (EAE) is an animal model of multiple sclerosis (MS), a human inflammatory and demyelinating disease. Microglia and astrocytes are glial cells of the central nervous system (CNS) that play a dual role in MS and EAE pathology. The aim of this study was to examine the effect of combined treatment with two nucleoside analogues, ribavirin and tiazofurin, on microglia and astrocytes in actively induced EAE. Therapeutic treatment with a combination of these two nucleoside analogues reduced disease severity, mononuclear cell infiltration and demyelination. The obtained histological results indicate that ribavirin and tiazofurin changed activated microglia into an inactive type and attenuated astrocyte reactivity at the end of the treatment period. Since reduction of reactive microgliosis and astrogliosis correlated with EAE suppression, the present study also suggests that the obtained beneficial effect of ribavirin and tiazofurin could be a consequence of their action inside as well as outside the CNS.",
journal = "Archives of Biological Sciences",
title = "Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis",
number = "3",
volume = "64",
pages = "843-850",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_317"
}

Savić, D., Lavrnja, I., Dacić, S., Bjelobaba, I., Nedeljković, N., Peković, S.,& Stojiljković, M.. (2012). Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis. in Archives of Biological Sciences, 64(3), 843-850.
https://hdl.handle.net/21.15107/rcub_ibiss_317

Savić D, Lavrnja I, Dacić S, Bjelobaba I, Nedeljković N, Peković S, Stojiljković M. Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis. in Archives of Biological Sciences. 2012;64(3):843-850.
https://hdl.handle.net/21.15107/rcub_ibiss_317 .

Savić, Danijela, Lavrnja, Irena, Dacić, Sanja, Bjelobaba, Ivana, Nedeljković, Nadežda, Peković, Sanja, Stojiljković, Mirjana, "Combined treatment with ribavirin and tiazofurin attenuates response of glial cells in experimental autoimmune encephalomyelitis" in Archives of Biological Sciences, 64, no. 3 (2012):843-850,
https://hdl.handle.net/21.15107/rcub_ibiss_317 .

TY  - JOUR
AU  - Dacić, Sanja
AU  - Peković, Sanja
AU  - Stojiljković, Maja T.
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Bjelobaba, Ivana
AU  - Stojiljković, Mirjana
PY  - 2008
PY  - 2008
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/207
AB  - The central nervous system has a limited capacity for self-repair after damage. However, the neonatal brain has agreater capacity for recovery than the adult brain. These differences in the regenerative capability depend on local environmental factors and the maturational stage of growing axons. Among molecules which have both growth-promoting and growth-inhibiting activities is the heterogeneous class of chondroitin sulfate proteoglycans (CSPGs). In this paper, we investigated the chondroitin-4 and chondroitin-6 sulfate proteoglycan expression profile after left sensorimotor cortex ablation of the neonatal and adult rat brain. Immunohistochemical analysis revealed that compared to the normal uninjured cortex, lesion provoked up regulation of CSPGs showing a different pattern of expression in the neonatal vs. the adult brain. Punctuate and membrane-bound labeling was predominate after neonatal lesion, where as heavy deposition of staining in the extracellular matrix was observed after adult lesion. Heavy deposition of CSPG immunoreactivity around the lesionsite in adult rats, in contrast to a less CSPG-rich environment in neonatal rats, indicated that enhancement of the recovery process after neonatal injury is due to amore permissive environment.
AB  - Centralni nervni sistem ima ograničen kapacitet za oporavak nakon povrede. Međutim, neonatalni mozak pokazuje veću sposobnost oporavka u odnosu na odrasle. Ove razlike zavise od lokalnih sredinskih faktora i stepena zrelosti aksona tokom izrastanja. U grupu molekula koji mogu da stimulišu ili inhibiraju rast aksona spada i heterogena klasa molekula označena kao hondroitin sulfatni proteoglikani (CSPG). U ovom radu ispitivanje profil ekspresije hondroitin-4 i hondroitin-6 sulfatnih proteoglikana nakonlezije leve senzomotorne kore neonatalnog i adultnog mozga pacova. Imunohistohemijska analiza pokazuje da u odnosu na normalni,nepovređeni korteks, lezija dovodi do povećanja ekspresije CSPG koji ima različiti obrazac promena u neonatalnom u odnosu na adultni mozak. Nakonlezije kod mladih, predominiraju tačkasta i membranski-vezana forma, dok kod odraslih lezija dovodi do nagomilavanja CSPG u ekstra ćelijskom matriksu. Prohodnija sredina u mozgu neonatalnih pacova koja je siromašnija CSPG, preduslov je boljeg procesa oporavka u odnosu na adulte, kod kojih se nakon povrede CSPG nagomilavaju oko mesta lezije.
T2  - Archives of Biological Sciences
T1  - Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova
T1  - Pattern of chondroitin sulfate proteoglycan expression after ablation of the sensorimotor cortex of the neonatal and adult rat brain
IS  - 4
VL  - 60
SP  - 581
EP  - 591
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_207
ER  - 

@article{
author = "Dacić, Sanja and Peković, Sanja and Stojiljković, Maja T. and Lavrnja, Irena and Savić, Danijela and Bjelobaba, Ivana and Stojiljković, Mirjana",
year = "2008, 2008",
abstract = "The central nervous system has a limited capacity for self-repair after damage. However, the neonatal brain has agreater capacity for recovery than the adult brain. These differences in the regenerative capability depend on local environmental factors and the maturational stage of growing axons. Among molecules which have both growth-promoting and growth-inhibiting activities is the heterogeneous class of chondroitin sulfate proteoglycans (CSPGs). In this paper, we investigated the chondroitin-4 and chondroitin-6 sulfate proteoglycan expression profile after left sensorimotor cortex ablation of the neonatal and adult rat brain. Immunohistochemical analysis revealed that compared to the normal uninjured cortex, lesion provoked up regulation of CSPGs showing a different pattern of expression in the neonatal vs. the adult brain. Punctuate and membrane-bound labeling was predominate after neonatal lesion, where as heavy deposition of staining in the extracellular matrix was observed after adult lesion. Heavy deposition of CSPG immunoreactivity around the lesionsite in adult rats, in contrast to a less CSPG-rich environment in neonatal rats, indicated that enhancement of the recovery process after neonatal injury is due to amore permissive environment., Centralni nervni sistem ima ograničen kapacitet za oporavak nakon povrede. Međutim, neonatalni mozak pokazuje veću sposobnost oporavka u odnosu na odrasle. Ove razlike zavise od lokalnih sredinskih faktora i stepena zrelosti aksona tokom izrastanja. U grupu molekula koji mogu da stimulišu ili inhibiraju rast aksona spada i heterogena klasa molekula označena kao hondroitin sulfatni proteoglikani (CSPG). U ovom radu ispitivanje profil ekspresije hondroitin-4 i hondroitin-6 sulfatnih proteoglikana nakonlezije leve senzomotorne kore neonatalnog i adultnog mozga pacova. Imunohistohemijska analiza pokazuje da u odnosu na normalni,nepovređeni korteks, lezija dovodi do povećanja ekspresije CSPG koji ima različiti obrazac promena u neonatalnom u odnosu na adultni mozak. Nakonlezije kod mladih, predominiraju tačkasta i membranski-vezana forma, dok kod odraslih lezija dovodi do nagomilavanja CSPG u ekstra ćelijskom matriksu. Prohodnija sredina u mozgu neonatalnih pacova koja je siromašnija CSPG, preduslov je boljeg procesa oporavka u odnosu na adulte, kod kojih se nakon povrede CSPG nagomilavaju oko mesta lezije.",
journal = "Archives of Biological Sciences",
title = "Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova, Pattern of chondroitin sulfate proteoglycan expression after ablation of the sensorimotor cortex of the neonatal and adult rat brain",
number = "4",
volume = "60",
pages = "581-591",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_207"
}

Dacić, S., Peković, S., Stojiljković, M. T., Lavrnja, I., Savić, D., Bjelobaba, I.,& Stojiljković, M.. (2008). Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova. in Archives of Biological Sciences, 60(4), 581-591.
https://hdl.handle.net/21.15107/rcub_ibiss_207

Dacić S, Peković S, Stojiljković MT, Lavrnja I, Savić D, Bjelobaba I, Stojiljković M. Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova. in Archives of Biological Sciences. 2008;60(4):581-591.
https://hdl.handle.net/21.15107/rcub_ibiss_207 .

Dacić, Sanja, Peković, Sanja, Stojiljković, Maja T., Lavrnja, Irena, Savić, Danijela, Bjelobaba, Ivana, Stojiljković, Mirjana, "Obrazac promena ekspresije hondroitin sulfatnih proteoglikana nakon ablacije senzomotornog korteksa kod mozga neonatalnih i odraslih pacova" in Archives of Biological Sciences, 60, no. 4 (2008):581-591,
https://hdl.handle.net/21.15107/rcub_ibiss_207 .

TY  - JOUR
AU  - Nedeljković, Nadežda
AU  - Bjelobaba, Ivana
AU  - Dacić, Sanja
AU  - Lavrnja, Irena
AU  - Peković, Sanja
AU  - Savić, Danijela
AU  - Vještica, Aleksandar
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2006
UR  - https://onlinelibrary.wiley.com/doi/abs/10.1016/j.cellbi.2006.03.001
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/3464
UR  - https://www.sciencedirect.com/science/article/abs/pii/S1065699506000643
AB  - The objective of this study was to examine the changes in the activity and expression of ectonucleotidase enzymes in the model of unilateral cortical stab injury (CSI) in rat. The activities of ecto-nucleoside triphosphate diphosphohydrolase 1 (NTPDase 1) and ecto 50-nucleotidase were assessed by measuring the levels of ATP, ADP and AMP hydrolysis in the crude membrane preparations obtained from injured left cortex, right cortex, left and right caudate nucleus, whole hippocampus and cerebellum. Significant increase in NTPDase and ecto 50-nucleotidase activities was observed in the injured cortex following CSI, whereas in other brain areas only an increase in ecto 50-nucleotidase activity was seen. Immunohistochemical analysis performed using antibodies specific to NTPDase 1 and ecto 50-nucleotidase demonstrated that CSI induced sig-nificant changes in enzyme expression around the injury site. Immunoreactivity patterns obtained for NTPDase 1 and ecto 50-nucleotidase were compared with those obtained for glial fibrillary acidic protein, as a marker of astrocytes and complement receptor type 3 (OX42), as a marker of microglia. Results suggest that up-regulation of ectonucleotidase after CSI is catalyzed by cells that activate in response to injury, i.e. cells immunopositive for NTPDase 1 were predominantly microglial cells, whereas cells immunopositive for ecto 50-nucleotidase were predominantly astrocytes.
PB  - Elsevier
T2  - Cell Biology International
T1  - Up-regulation of ectonucleotidase activity after cortical stab injury in rats
IS  - 6
VL  - 30
DO  - 10.1016/j.cellbi.2006.03.001
SP  - 541
EP  - 546
ER  - 

@article{
author = "Nedeljković, Nadežda and Bjelobaba, Ivana and Dacić, Sanja and Lavrnja, Irena and Peković, Sanja and Savić, Danijela and Vještica, Aleksandar and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2006",
abstract = "The objective of this study was to examine the changes in the activity and expression of ectonucleotidase enzymes in the model of unilateral cortical stab injury (CSI) in rat. The activities of ecto-nucleoside triphosphate diphosphohydrolase 1 (NTPDase 1) and ecto 50-nucleotidase were assessed by measuring the levels of ATP, ADP and AMP hydrolysis in the crude membrane preparations obtained from injured left cortex, right cortex, left and right caudate nucleus, whole hippocampus and cerebellum. Significant increase in NTPDase and ecto 50-nucleotidase activities was observed in the injured cortex following CSI, whereas in other brain areas only an increase in ecto 50-nucleotidase activity was seen. Immunohistochemical analysis performed using antibodies specific to NTPDase 1 and ecto 50-nucleotidase demonstrated that CSI induced sig-nificant changes in enzyme expression around the injury site. Immunoreactivity patterns obtained for NTPDase 1 and ecto 50-nucleotidase were compared with those obtained for glial fibrillary acidic protein, as a marker of astrocytes and complement receptor type 3 (OX42), as a marker of microglia. Results suggest that up-regulation of ectonucleotidase after CSI is catalyzed by cells that activate in response to injury, i.e. cells immunopositive for NTPDase 1 were predominantly microglial cells, whereas cells immunopositive for ecto 50-nucleotidase were predominantly astrocytes.",
publisher = "Elsevier",
journal = "Cell Biology International",
title = "Up-regulation of ectonucleotidase activity after cortical stab injury in rats",
number = "6",
volume = "30",
doi = "10.1016/j.cellbi.2006.03.001",
pages = "541-546"
}

Nedeljković, N., Bjelobaba, I., Dacić, S., Lavrnja, I., Peković, S., Savić, D., Vještica, A., Rakić, L.,& Stojiljković, M.. (2006). Up-regulation of ectonucleotidase activity after cortical stab injury in rats. in Cell Biology International
Elsevier., 30(6), 541-546.
https://doi.org/10.1016/j.cellbi.2006.03.001

Nedeljković N, Bjelobaba I, Dacić S, Lavrnja I, Peković S, Savić D, Vještica A, Rakić L, Stojiljković M. Up-regulation of ectonucleotidase activity after cortical stab injury in rats. in Cell Biology International. 2006;30(6):541-546.
doi:10.1016/j.cellbi.2006.03.001 .

Nedeljković, Nadežda, Bjelobaba, Ivana, Dacić, Sanja, Lavrnja, Irena, Peković, Sanja, Savić, Danijela, Vještica, Aleksandar, Rakić, Ljubisav, Stojiljković, Mirjana, "Up-regulation of ectonucleotidase activity after cortical stab injury in rats" in Cell Biology International, 30, no. 6 (2006):541-546,
https://doi.org/10.1016/j.cellbi.2006.03.001 . .

TY  - CHAP
AU  - Peković, Sanja
AU  - Dacić, Sanja
AU  - Nedeljković, Nadežda
AU  - Bjelobaba, Ivana
AU  - Filipović, Radmila
AU  - Milenković, Ivan
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Jovanović, Saša
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2006
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5871
AB  - Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.
PB  - Kerala, India: Research Signpost
T2  - Neurobiological studies – From genes to behavior 2006
T1  - Molecular basis of brain injury and repair
SP  - 143
EP  - 165
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_5871
ER  - 

@inbook{
author = "Peković, Sanja and Dacić, Sanja and Nedeljković, Nadežda and Bjelobaba, Ivana and Filipović, Radmila and Milenković, Ivan and Lavrnja, Irena and Savić, Danijela and Jovanović, Saša and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2006",
abstract = "Injury to the central nervous system (CNS) is one of the leading causes of death and invalidity among all people below the age of 45 for which there are no specific treatments. The insight into the molecular pathophysiology of brain dysfunctions after the injury will provide indications for new effective therapeutic approaches that will limit damage, slow cell death and promote repair. The aim of this review is to highlight molecular mechanisms underlining primary and secondary injury. The initial impact or primary injury induces elevation of extracellular concentration of neurotransmitters leading to changes in electrical properties of neuronal membrane, net influx of Ca2+ and activation of diverse cellular signaling pathways. To restore neuronal homeostasis, the activities and expression of a variety of enzymes involved in control of extracellular concentration of biogenic amines and purine nucleotides/nucleosides, as well as the membrane potential are altered. The CNS has a limited capacity of self-repair. However, there are indications that the neonatal brain has a greater capacity for recovery than adult brain. The well known pathological hallmark of CNS injury is formation of the glial scar, the major impediment to axonal regeneration. Recently, it was shown that treatment with the purine nucleoside analogues attenuates and delays the process of reactive gliosis, and thus may be a useful approach for improving neurological recovery from head injury.",
publisher = "Kerala, India: Research Signpost",
journal = "Neurobiological studies – From genes to behavior 2006",
booktitle = "Molecular basis of brain injury and repair",
pages = "143-165",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_5871"
}

Peković, S., Dacić, S., Nedeljković, N., Bjelobaba, I., Filipović, R., Milenković, I., Lavrnja, I., Savić, D., Jovanović, S., Rakić, L.,& Stojiljković, M.. (2006). Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006
Kerala, India: Research Signpost., 143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871

Peković S, Dacić S, Nedeljković N, Bjelobaba I, Filipović R, Milenković I, Lavrnja I, Savić D, Jovanović S, Rakić L, Stojiljković M. Molecular basis of brain injury and repair. in Neurobiological studies – From genes to behavior 2006. 2006;:143-165.
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .

Peković, Sanja, Dacić, Sanja, Nedeljković, Nadežda, Bjelobaba, Ivana, Filipović, Radmila, Milenković, Ivan, Lavrnja, Irena, Savić, Danijela, Jovanović, Saša, Rakić, Ljubisav, Stojiljković, Mirjana, "Molecular basis of brain injury and repair" in Neurobiological studies – From genes to behavior 2006 (2006):143-165,
https://hdl.handle.net/21.15107/rcub_ibiss_5871 .

TY  - JOUR
AU  - Peković, Sanja
AU  - Filipović, Radmila
AU  - Dacić, Sanja
AU  - Lavrnja, Irena
AU  - Savić, Danijela
AU  - Nedeljković, Nadežda
AU  - Rakić, Ljubisav
AU  - Stojiljković, Mirjana
PY  - 2005
UR  - http://radar.ibiss.bg.ac.rs/handle/123456789/5870
AB  - The weak regenerative capacity of self-repair after injury to the adult brain is caused by the formation of glial sear due to reactive astrogliosis. In the present study the beginning of reactive astrogliosis in the adult, as shown immunocytochemically by upregulation of glial fibrillary acidic protein (GFAP) and vimentin, was seen two days after the left sensorimotor cortex lesion, being maximal during the first two weeks and declining by 30 days after the lesion. This was accompanied by intensive glial scarring. Conversely, after the neonatal lesion a lack of gliotic scar was seen until 30 days postsurgery, although the pattern of GFAP and vimentin expression during recovery period was the same. The aim of the study was to define an appropriate therapeutic intervention that could modulate astrocyte proliferation and diminish glial scar formation after adult brain lesion. For this purpose the effects of an antiproliferative agent, the purine nucleoside analogue ribavirin was examined. It was shown that daily injection of ribavirin for 5 and 10 days considerably decreased the number of reactive astrocytes, while slight GFAP labeling was restricted to the lesion site. Obtained results show that ribavirin treatment downregulates the process of reactive astrogliosis after adult brain injury, and thus may be a useful approach for improving neurological recovery from brain damage.
PB  - Hoboken, NJ: Wiley
T2  - Annals of the New York Academy of Sciences
T1  - Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin
IS  - 1
VL  - 1048
DO  - 10.1196/annals.1342.027
SP  - 296
EP  - 310
ER  - 

@article{
author = "Peković, Sanja and Filipović, Radmila and Dacić, Sanja and Lavrnja, Irena and Savić, Danijela and Nedeljković, Nadežda and Rakić, Ljubisav and Stojiljković, Mirjana",
year = "2005",
abstract = "The weak regenerative capacity of self-repair after injury to the adult brain is caused by the formation of glial sear due to reactive astrogliosis. In the present study the beginning of reactive astrogliosis in the adult, as shown immunocytochemically by upregulation of glial fibrillary acidic protein (GFAP) and vimentin, was seen two days after the left sensorimotor cortex lesion, being maximal during the first two weeks and declining by 30 days after the lesion. This was accompanied by intensive glial scarring. Conversely, after the neonatal lesion a lack of gliotic scar was seen until 30 days postsurgery, although the pattern of GFAP and vimentin expression during recovery period was the same. The aim of the study was to define an appropriate therapeutic intervention that could modulate astrocyte proliferation and diminish glial scar formation after adult brain lesion. For this purpose the effects of an antiproliferative agent, the purine nucleoside analogue ribavirin was examined. It was shown that daily injection of ribavirin for 5 and 10 days considerably decreased the number of reactive astrocytes, while slight GFAP labeling was restricted to the lesion site. Obtained results show that ribavirin treatment downregulates the process of reactive astrogliosis after adult brain injury, and thus may be a useful approach for improving neurological recovery from brain damage.",
publisher = "Hoboken, NJ: Wiley",
journal = "Annals of the New York Academy of Sciences",
title = "Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin",
number = "1",
volume = "1048",
doi = "10.1196/annals.1342.027",
pages = "296-310"
}

Peković, S., Filipović, R., Dacić, S., Lavrnja, I., Savić, D., Nedeljković, N., Rakić, L.,& Stojiljković, M.. (2005). Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin. in Annals of the New York Academy of Sciences
Hoboken, NJ: Wiley., 1048(1), 296-310.
https://doi.org/10.1196/annals.1342.027

Peković S, Filipović R, Dacić S, Lavrnja I, Savić D, Nedeljković N, Rakić L, Stojiljković M. Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin. in Annals of the New York Academy of Sciences. 2005;1048(1):296-310.
doi:10.1196/annals.1342.027 .

Peković, Sanja, Filipović, Radmila, Dacić, Sanja, Lavrnja, Irena, Savić, Danijela, Nedeljković, Nadežda, Rakić, Ljubisav, Stojiljković, Mirjana, "Downregulation of Glial Scarring after Brain Injury: The Effect of Purine Nucleoside Analogue Ribavirin" in Annals of the New York Academy of Sciences, 1048, no. 1 (2005):296-310,
https://doi.org/10.1196/annals.1342.027 . .