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缺血预处理诱导小鼠脑内少突胶质前体细胞发生:Nrf2 缺乏的影响。

Ischemic Preconditioning Induces Oligodendrogenesis in Mouse Brain: Effects of Nrf2 Deficiency.

机构信息

Department of Neurology, The Second Affiliated Hospital of Zhengzhou University, Zhengzhou, Henan, China.

Department of Neurology, Pittsburgh Institute of Brain Disorders and Recovery, University of Pittsburgh School of Medicine, Pittsburgh, PA, USA.

出版信息

Cell Mol Neurobiol. 2022 Aug;42(6):1859-1873. doi: 10.1007/s10571-021-01068-5. Epub 2021 Mar 5.

Abstract

Ischemic preconditioning (IPC) is an approach of protection against cerebral ischemia by inducing endogenous cytoprotective machinery. However, few studies in neurogenesis and oligodendrogenesis after IPC have been reported, especially the latter. The purpose of this study is to test our hypothesis that IPC may also induce cell proliferation and oligodendrogenesis in the subventricular zone and striatum, as well as to investigate the effect of nuclear factor erythroid 2-related factor 2 (Nrf2) on oligodendrogenesis. IPC was induced in mice by 12-min ischemia through the occlusion of the middle cerebral artery. Newly generated cells were labeled with 5-bromo-2'-deoxyuridine. Our findings demonstrated that IPC stimulated the proliferation of neural stem cells in the subventricular zone, promoted the generation of oligodendrocyte precursor cells in the striatum and corpus callosum/external capsule (CC/EC), and stimulated oligodendrocyte precursor cells differentiation into oligodendrocytes in the striatum and the CC/EC. Furthermore, we describe a crucial role for Nrf2 in IPC-induced oligodendrogenesis in the subventricular zone, striatum, and CC/EC and show for the first time that Nrf2 promoted the migration and differentiation of oligodendrocyte precursor cells into oligodendrocytes in the striatum and CC/EC. Our data imply that IPC stimulates the oligodendrogenesis in the brain and that Nrf2 signaling may contribute to the oligodendrogenesis.

摘要

缺血预处理(IPC)是一种通过诱导内源性保护机制来防止脑缺血的保护方法。然而,仅有少数关于 IPC 后神经发生和少突胶质细胞发生的研究报道,尤其是后者。本研究旨在验证我们的假设,即 IPC 也可能诱导侧脑室和纹状体中的细胞增殖和少突胶质细胞发生,并研究核因子红细胞 2 相关因子 2(Nrf2)对少突胶质细胞发生的影响。通过大脑中动脉闭塞实现 12 分钟的缺血来诱导 IPC。用 5-溴-2'-脱氧尿苷标记新生成的细胞。我们的研究结果表明,IPC 刺激侧脑室中的神经干细胞增殖,促进纹状体和胼胝体/外囊(CC/EC)中少突胶质前体细胞的生成,并刺激少突胶质前体细胞在纹状体和 CC/EC 中分化为少突胶质细胞。此外,我们描述了 Nrf2 在 IPC 诱导的侧脑室、纹状体和 CC/EC 中的少突胶质细胞发生中的关键作用,并首次表明 Nrf2 促进了少突胶质前体细胞在纹状体和 CC/EC 中的迁移和分化为少突胶质细胞。我们的数据表明,IPC 刺激大脑中的少突胶质细胞发生,而 Nrf2 信号可能有助于少突胶质细胞发生。

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