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L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury
dc.contributor | Isaković, Anđelka | |
dc.creator | Dacić, Sanja | |
dc.creator | Božić, Iva | |
dc.creator | Jeremić, Rada | |
dc.creator | Bjelobaba, Ivana | |
dc.creator | Lavrnja, Irena | |
dc.creator | Savić, Danijela | |
dc.creator | Rakić, Ljubisav | |
dc.creator | Stojiljković, Mirjana | |
dc.creator | Peković, Sanja | |
dc.date.accessioned | 2023-07-27T11:41:25Z | |
dc.date.available | 2023-07-27T11:41:25Z | |
dc.date.issued | 2019 | |
dc.identifier.isbn | 978-86-917255-3-2 | |
dc.identifier.uri | http://radar.ibiss.bg.ac.rs/handle/123456789/5989 | |
dc.description.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. | sr |
dc.language.iso | en | sr |
dc.publisher | Belgrade: Serbian Neuroscience Society | sr |
dc.relation | info:eu-repo/grantAgreement/MESTD/Integrated and Interdisciplinary Research (IIR or III)/41014/RS// | sr |
dc.rights | openAccess | sr |
dc.source | Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia | sr |
dc.title | L-type Calcium Channels Involvement in the Regulation of Neuroinflammation and Neuroregeneration After Brain Injury | sr |
dc.type | article | sr |
dc.rights.license | ARR | sr |
dc.rights.holder | © 2019 by the Serbian Neuroscience Society | sr |
dc.description.other | Isaković A, editor. Book of Abstract: Federation of European Neuroscience Societies (FENS) Regional Meeting; 2019 Jul 10-13; Belgrade, Serbia. Belgrade: Serbian Neuroscience Society; 2019. p. 487. | sr |
dc.citation.spage | 487 | |
dc.type.version | publishedVersion | sr |
dc.identifier.cobiss | 282222604 | |
dc.identifier.fulltext | https://radar.ibiss.bg.ac.rs/bitstream/id/14256/FRM2019_P262.pdf | |
dc.citation.rank | M34 | |
dc.identifier.rcub | https://hdl.handle.net/21.15107/rcub_ibiss_5989 |