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Cav3.2 channel regulates cerebral ischemia/reperfusion injury: a promising target for intervention.
Dai, Feibiao; Hu, Chengyun; Li, Xue; Zhang, Zhetao; Wang, Hongtao; Zhou, Wanjun; Wang, Jiawu; Geng, Qingtian; Dong, Yongfei; Tang, Chaoliang.
Afiliação
  • Dai F; Graduate School, Wannan Medical College, Wuhu, Anhui Province, China.
  • Hu C; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui Province, China.
  • Li X; Core Facility Center for Medical Sciences, The First Affiliated Hospital of USTC (Anhui Provincial Hospital), Hefei, Anhui Province, China.
  • Zhang Z; Graduate School, Wannan Medical College, Wuhu, Anhui Province, China.
  • Wang H; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui Province, China.
  • Zhou W; Core Facility Center for Medical Sciences, The First Affiliated Hospital of USTC (Anhui Provincial Hospital), Hefei, Anhui Province, China.
  • Wang J; Graduate School, Wannan Medical College, Wuhu, Anhui Province, China.
  • Geng Q; Department of Anesthesiology, The First Affiliated Hospital of USTC, Division of Life Sciences and Medicine, University of Science and Technology of China, Hefei, Anhui Province, China.
  • Dong Y; Core Facility Center for Medical Sciences, The First Affiliated Hospital of USTC (Anhui Provincial Hospital), Hefei, Anhui Province, China.
  • Tang C; Core Facility Center for Medical Sciences, The First Affiliated Hospital of USTC (Anhui Provincial Hospital), Hefei, Anhui Province, China.
Neural Regen Res ; 19(11): 2480-2487, 2024 Nov 01.
Article em En | MEDLINE | ID: mdl-38526284
ABSTRACT
JOURNAL/nrgr/04.03/01300535-202419110-00028/figure1/v/2024-03-08T184507Z/r/image-tiff Calcium influx into neurons triggers neuronal death during cerebral ischemia/reperfusion injury. Various calcium channels are involved in cerebral ischemia/reperfusion injury. Cav3.2 channel is a main subtype of T-type calcium channels. T-type calcium channel blockers, such as pimozide and mibefradil, have been shown to prevent cerebral ischemia/reperfusion injury-induced brain injury. However, the role of Cav3.2 channels in cerebral ischemia/reperfusion injury remains unclear. Here, in vitro and in vivo models of cerebral ischemia/reperfusion injury were established using middle cerebral artery occlusion in mice and high glucose hypoxia/reoxygenation exposure in primary hippocampal neurons. The results showed that Cav3.2 expression was significantly upregulated in injured hippocampal tissue and primary hippocampal neurons. We further established a Cav3.2 gene-knockout mouse model of cerebral ischemia/reperfusion injury. Cav3.2 knockout markedly reduced infarct volume and brain water content, and alleviated neurological dysfunction after cerebral ischemia/reperfusion injury. Additionally, Cav3.2 knockout attenuated cerebral ischemia/reperfusion injury-induced oxidative stress, inflammatory response, and neuronal apoptosis. In the hippocampus of Cav3.2-knockout mice, calcineurin overexpression offset the beneficial effect of Cav3.2 knockout after cerebral ischemia/reperfusion injury. These findings suggest that the neuroprotective function of Cav3.2 knockout is mediated by calcineurin/nuclear factor of activated T cells 3 signaling. Findings from this study suggest that Cav3.2 could be a promising target for treatment of cerebral ischemia/reperfusion injury.

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Neural Regen Res Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Idioma: En Revista: Neural Regen Res Ano de publicação: 2024 Tipo de documento: Article País de afiliação: China