ArticleCellular and molecular neurobiology2013
The role of connexin 43 and hemichannels correlated with the astrocytic death following ischemia/reperfusion insult.
Article in Cellular and molecular neurobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 22 citations in OpenAlex.
- Regulation of the Angiogenic Potential of Endothelial Cells In Vitro under Conditions of Acute Hypoxic Stress: The Role of Homotypic Communication via Gap Junctions.Bulletin of experimental biology and medicine · 2025Article
- Connexin43 in Post-Surgical Peritoneal Adhesion Formation.Life (Basel, Switzerland) · 2022Article
- Apoptotic Osteocytes Induce RANKL Production in Bystanders via Purinergic Signaling and Activation of Pannexin Channels.Journal of bone and mineral research : the official journal of the American Society for Bone and Mineral Research · 2020Article
- Evaluation of Connexin 43 Redistribution and Endocytosis in Astrocytes Subjected to Ischemia/Reperfusion or Oxygen-Glucose Deprivation and Reoxygenation.BioMed research international · 2017Article
- Gap Junction Intercellular Communication Mediates Ammonia-Induced Neurotoxicity.Neurotoxicity research · 2016Article
- Isoform-specific phosphorylation-dependent regulation of connexin hemichannels.Journal of neurophysiology · 2015Article
- Connexin: a potential novel target for protecting the central nervous system?Neural regeneration research · 2015Review
- Intracellular Cleavage of the Cx43 C-Terminal Domain by Matrix-Metalloproteases: A Novel Contributor to Inflammation?Mediators of inflammation · 2015Review
- Connexin hemichannel blockade is neuroprotective after asphyxia in preterm fetal sheep.PloS one · 2014Article
- Neurological manifestations of oculodentodigital dysplasia: a Cx43 channelopathy of the central nervous system?Frontiers in pharmacology · 2013Review
- Connexin 43 and Its Hemichannels Mediate Hypoxia-Ischemia-Induced Cell Death in Neonatal Rats.Child neurology openArticle
Corrections and comments
- Erratum issuedBecker, David L [removed]
Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The aim of this study was to investigate the role of connexin 43 (Cx43) and its hemichannel (HC1) in the death of astrocytes following ischemia/reperfusion (IR) or oxygen-glucose deprivation/reoxygenation (OGDR) insult. Wistar rats had their bilateral common carotid artery clamped for 1.5 h followed by 0, 4, and 24 h of reperfusion (n = 8 for each time point), respectively. All rats were sacrificed and Cx43, HC1, and caspase 3 (Casp3) in cerebral ischemic tissues were examined by immunohistochemistry and western blotting. Astrocytes cell line, astrocytes transduced with a retroviral empty vector (Psup astrocyte), or a Cx43-specific shRNA construct (shRNA astrocytes) were treated with OGDR insult for various periods. The viability of astrocytes was assessed by MTT assay. The expression of Cx43, HC1, and Casp3 was detected with western blotting. The results showed that the expression of Cx43, HC1, and Casp3 in rats' brain, astrocytes, and Psup astrocytes was significantly increased after 4 h of IR/OGDR and recovered on 24 h of the insult. Cell viability decreased after 4 h of the insult whereas the cell viability increased on 24 h after the insult. In contrast, the expression of Cx43, HC1, Casp3, and cell viability had no statistical differences in the null Cx43 gene-shRNA transfected astrocytes after the treatment of OGDR. The results suggest that Cx43 and HC1 are likely to play the pivotal roles in the mediation of the astrocytic death.
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