Rakić, Ljubisav

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  • Rakić, Ljubisav (5)
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Author's Bibliography

L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury

Dacić, Sanja; Božić, Iva; Jeremić, Rada; Bjelobaba, Ivana; Lavrnja, Irena; Savić, Danijela; Rakić, Ljubisav; Stojiljković, Mirjana; Peković, Sanja

(Belgrade: Serbian Neuroscience Society, 2019)

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 .

Preusmeravanje antivirusnog leka ribavirina ka novim terapijskim indikacijama: primer multiple skleroze i neoplastičnih transformacija

Savić, Danijela; Lavrnja, Irena; Bjelobaba, Ivana; Dacić, Sanja; Laketa, Danijela; Božić, Iva; Jakovljević, Marija; Nedeljković, Nadežda; Rakić, Ljubisav; Peković, Sanja

(Belgrade: Serbian Biological Society, 2018)

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 .

Molecular basis of brain injury and repair

Peković, Sanja; Dacić, Sanja; Nedeljković, Nadežda; Bjelobaba, Ivana; Filipović, Radmila; Milenković, Ivan; Lavrnja, Irena; Savić, Danijela; Jovanović, Saša; Rakić, Ljubisav; Stojiljković, Mirjana

(Kerala, India: Research Signpost, 2006)

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 .
5

Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro

Janković, Dragana; Stojković, Ana; Pešić, Milica; Kanazir, Selma; Rakić, Ljubisav; Ruždijić, Sabera D.

(2004)

TY  - JOUR
AU  - Janković, Dragana
AU  - Stojković, Ana
AU  - Pešić, Milica
AU  - Kanazir, Selma
AU  - Rakić, Ljubisav
AU  - Ruždijić, Sabera D.
PY  - 2004
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/31
AB  - Angiogenesis is essential for tumor growth and relies on the production of angiogenic factors. By comparative analysis using RT-PCR method of angiogenic growth factors: VEGF, bFGF, PDGF-A, angiogenin- 1 and IL-8 we established the level of expression of these genes necessary for angiogenesis in glioma and neuroblastoma cell lines. Our analyses were also extended to CD44 gene, which plays an important role in cascade of metastasis and progression of brain tumors. Significant differences in the level of gene expression of angiogenic factors and CD44 gene between the two cell lines observed throughout this study can be used as a prognostic marker for predicting clinical outcome in human brain tumors at the time of the initial staging.
AB  - Angiogeneza je neophodna za rast tumora i zahteva proizvodnju angiogenih trofičkih faktora koji učestvuju u tumorogenezi. Uporednom analizom angiogenih trofičkih faktora: VEGF, bFGF, PDGF-A, angiogenina-1 i IL-8 pomoću metode RT-PCR utvrdili smo nivo ekspresije ovih gena uključenih u proces angiogeneze u ćelijskim linijama glioma i neuroblastoma. Takođe smo proširili analize i na CD44 gen koji igra važnu ulogu u kaskadi nastanka i progresiji metastaza tumora mozga. Dobijeni rezultati ukazuju na značajnu razliku u nivou genske ekspresije angiogenih faktora i CD44 gena u ove dve ćelijske linije čije se poreklo razlikuje ne samo po nastanku već i po mestu rasejavnja metastaza. Rezultati bi mogli da posluže kao prognostički faktor u prekliničkim i kliničkim istraživanjima tumora mozga od inicijalnih do terminalnih stupnjeva nastanka i terapije.
T2  - Jugoslovenska medicinska biohemija
T1  - Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro
T1  - Comparative analysis of expression of angiogenic factors and CD44 gene in human glioma and neuroblastoma cell lines in vitro
IS  - 1
VL  - 23
SP  - 19
EP  - 24
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_31
ER  - 
@article{
author = "Janković, Dragana and Stojković, Ana and Pešić, Milica and Kanazir, Selma and Rakić, Ljubisav and Ruždijić, Sabera D.",
year = "2004",
abstract = "Angiogenesis is essential for tumor growth and relies on the production of angiogenic factors. By comparative analysis using RT-PCR method of angiogenic growth factors: VEGF, bFGF, PDGF-A, angiogenin- 1 and IL-8 we established the level of expression of these genes necessary for angiogenesis in glioma and neuroblastoma cell lines. Our analyses were also extended to CD44 gene, which plays an important role in cascade of metastasis and progression of brain tumors. Significant differences in the level of gene expression of angiogenic factors and CD44 gene between the two cell lines observed throughout this study can be used as a prognostic marker for predicting clinical outcome in human brain tumors at the time of the initial staging., Angiogeneza je neophodna za rast tumora i zahteva proizvodnju angiogenih trofičkih faktora koji učestvuju u tumorogenezi. Uporednom analizom angiogenih trofičkih faktora: VEGF, bFGF, PDGF-A, angiogenina-1 i IL-8 pomoću metode RT-PCR utvrdili smo nivo ekspresije ovih gena uključenih u proces angiogeneze u ćelijskim linijama glioma i neuroblastoma. Takođe smo proširili analize i na CD44 gen koji igra važnu ulogu u kaskadi nastanka i progresiji metastaza tumora mozga. Dobijeni rezultati ukazuju na značajnu razliku u nivou genske ekspresije angiogenih faktora i CD44 gena u ove dve ćelijske linije čije se poreklo razlikuje ne samo po nastanku već i po mestu rasejavnja metastaza. Rezultati bi mogli da posluže kao prognostički faktor u prekliničkim i kliničkim istraživanjima tumora mozga od inicijalnih do terminalnih stupnjeva nastanka i terapije.",
journal = "Jugoslovenska medicinska biohemija",
title = "Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro, Comparative analysis of expression of angiogenic factors and CD44 gene in human glioma and neuroblastoma cell lines in vitro",
number = "1",
volume = "23",
pages = "19-24",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_31"
}
Janković, D., Stojković, A., Pešić, M., Kanazir, S., Rakić, L.,& Ruždijić, S. D.. (2004). Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro. in Jugoslovenska medicinska biohemija, 23(1), 19-24.
https://hdl.handle.net/21.15107/rcub_ibiss_31
Janković D, Stojković A, Pešić M, Kanazir S, Rakić L, Ruždijić SD. Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro. in Jugoslovenska medicinska biohemija. 2004;23(1):19-24.
https://hdl.handle.net/21.15107/rcub_ibiss_31 .
Janković, Dragana, Stojković, Ana, Pešić, Milica, Kanazir, Selma, Rakić, Ljubisav, Ruždijić, Sabera D., "Uporedna analiza ekspresije angiogenih faktora i CD44 gena u humanim ćelijskim linijama glioma i neuroblastoma in vitro" in Jugoslovenska medicinska biohemija, 23, no. 1 (2004):19-24,
https://hdl.handle.net/21.15107/rcub_ibiss_31 .

6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova

Mladenović, Aleksandra; Perović, Milka; Milanović, Desanka; Kanazir, Selma; Rakić, Ljubisav; Ruždijić, Sabera

(2002)

TY  - JOUR
AU  - Mladenović, Aleksandra
AU  - Perović, Milka
AU  - Milanović, Desanka
AU  - Kanazir, Selma
AU  - Rakić, Ljubisav
AU  - Ruždijić, Sabera
PY  - 2002
UR  - https://radar.ibiss.bg.ac.rs/handle/123456789/21
AB  - The effects of four-site intrastriatal 6-hydroxydopamine (6-OHDA) lesions were examined in adult male rats. Five days after the lesions the animals were checked for specific rotational behavior induced by middle dose of amphetamine and the results confirmed the effectiveness of the lesions. The RNAs from the striatum were isolated at different time points after the lesion, and the RT-PCR analyse were performed for the D1 and D2 receptor mRNA. The results show a decline in the D2 receptor mRNA level (40%) at 6 h and 24 h points while this change was not observed seven days after the lesion. In contrast, no statistically significant changes in the level of the D1 receptor mRNA after the lesion at any time point were found.
AB  - Ispitivani su efekti četiri ubodne 6-hidroksidopaminske (6-OHDA) lezije striatuma kod odraslih mužjaka pacova. Pet dana nakon lezije, životinje su testirane na specifično rotaciono ponaš anje pod uticajem srednje doze amfetamina i rezultati su potvrdili efikasnost lezije. RNK iz striatuma su izolovane u različitim vremenskim tačkama nakon lezije i urađena je RT-PCR analiza iRNK za D1 i D2 dopaminske receptore. Rezultati pokazuju smanjivanje nivoa iRNK za D2 receptor (40%) 6 h i 24 h nakon lezije, dok sedam dana nakon lezije nema promena. Za razliku od ovih rezultata, u nivou iRNK za D1 receptor ne postoje statistički značajne razlike u bilo kojoj vremenskoj tački.
T2  - Jugoslovenska medicinska biohemija
T1  - 6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova
T1  - 6-hydroxydopamine lesions of the striatum lead to the alterations of dopamine receptor mrna in parkinsonian rats
IS  - 3
VL  - 21
DO  - 10.2298/JMH0203275M
SP  - 275
EP  - 282
UR  - https://hdl.handle.net/21.15107/rcub_ibiss_21
ER  - 
@article{
author = "Mladenović, Aleksandra and Perović, Milka and Milanović, Desanka and Kanazir, Selma and Rakić, Ljubisav and Ruždijić, Sabera",
year = "2002",
abstract = "The effects of four-site intrastriatal 6-hydroxydopamine (6-OHDA) lesions were examined in adult male rats. Five days after the lesions the animals were checked for specific rotational behavior induced by middle dose of amphetamine and the results confirmed the effectiveness of the lesions. The RNAs from the striatum were isolated at different time points after the lesion, and the RT-PCR analyse were performed for the D1 and D2 receptor mRNA. The results show a decline in the D2 receptor mRNA level (40%) at 6 h and 24 h points while this change was not observed seven days after the lesion. In contrast, no statistically significant changes in the level of the D1 receptor mRNA after the lesion at any time point were found., Ispitivani su efekti četiri ubodne 6-hidroksidopaminske (6-OHDA) lezije striatuma kod odraslih mužjaka pacova. Pet dana nakon lezije, životinje su testirane na specifično rotaciono ponaš anje pod uticajem srednje doze amfetamina i rezultati su potvrdili efikasnost lezije. RNK iz striatuma su izolovane u različitim vremenskim tačkama nakon lezije i urađena je RT-PCR analiza iRNK za D1 i D2 dopaminske receptore. Rezultati pokazuju smanjivanje nivoa iRNK za D2 receptor (40%) 6 h i 24 h nakon lezije, dok sedam dana nakon lezije nema promena. Za razliku od ovih rezultata, u nivou iRNK za D1 receptor ne postoje statistički značajne razlike u bilo kojoj vremenskoj tački.",
journal = "Jugoslovenska medicinska biohemija",
title = "6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova, 6-hydroxydopamine lesions of the striatum lead to the alterations of dopamine receptor mrna in parkinsonian rats",
number = "3",
volume = "21",
doi = "10.2298/JMH0203275M",
pages = "275-282",
url = "https://hdl.handle.net/21.15107/rcub_ibiss_21"
}
Mladenović, A., Perović, M., Milanović, D., Kanazir, S., Rakić, L.,& Ruždijić, S.. (2002). 6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova. in Jugoslovenska medicinska biohemija, 21(3), 275-282.
https://doi.org/10.2298/JMH0203275M
https://hdl.handle.net/21.15107/rcub_ibiss_21
Mladenović A, Perović M, Milanović D, Kanazir S, Rakić L, Ruždijić S. 6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova. in Jugoslovenska medicinska biohemija. 2002;21(3):275-282.
doi:10.2298/JMH0203275M
https://hdl.handle.net/21.15107/rcub_ibiss_21 .
Mladenović, Aleksandra, Perović, Milka, Milanović, Desanka, Kanazir, Selma, Rakić, Ljubisav, Ruždijić, Sabera, "6-hidroksidopaminska lezija striatuma izaziva promene irnk za dopaminske receptore kod parkisoničnog pacova" in Jugoslovenska medicinska biohemija, 21, no. 3 (2002):275-282,
https://doi.org/10.2298/JMH0203275M .,
https://hdl.handle.net/21.15107/rcub_ibiss_21 .
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