• Shumeng Li, Yiheng Li, Pengcheng Huang, Xiaocheng Mao, Kaiyan Jiang, Ran Chen, Qing Li, Lulu Wang, Zeqing Jin, Chenyi Wan, Ying Xiong, Yaqing Yu, Wenli Sheng, Daojun Hong, and Jing Lin.
• Department of Neurology, The First Affiliated Hospital of Nanchang University, Nanchang, Jiangxi, China.
• Neuroscience. 2023 Nov 21; 533: 102110-21.

AbstractPrevious studies by us and others have shown that RING finger protein 213 (RNF213) is associated with cerebrovascular disease and systemic vasculopathy. Indeed, Rnf213 mRNA expression is increased in cerebral ischemia reperfusion injury (CIRI). The purpose of the present study was to investigate the role of Rnf213 in CIRI. Using the middle cerebral artery occlusion (MCAO) model, we confirmed that the expression of RNF213 protein was significantly upregulated in neurons in the ischemic penumbra. Rnf213 knockout mice were successfully generated using CRISPR/Cas9 technology. According to TTC staining and Bederson neurological scale, removal of Rnf213 decreased brain infarct volume and improved neurological deficit score, although the restoration of cerebral blood flow after MCAO was similar in WT and Rnf213-/- mice. In addition, the levels of p-Akt, p-GSK-3β, β-catenin and Bcl-2 were significantly increased 24 h after MCAO in the ischemic penumbra of the Rnf213-/- mice compared to WT mice, indicating that Rnf213 removal may ameliorate neuronal apoptosis by regulating the Akt/GSK-3β/β-catenin/Bcl-2 signaling pathway. Taken together, our study reveals that Rnf213 regulates neuronal apoptosis in CIRI, therefore impacting on brain infarct volume in brain ischemia.Copyright © 2023 IBRO. Published by Elsevier Ltd. All rights reserved.

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