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G 蛋白偶联受体 GPR37L1 调控成体少突胶质细胞的生成。

G protein-coupled receptor GPR37-like 1 regulates adult oligodendrocyte generation.

机构信息

Faculty of Medical Sciences, Division of Medicine, Wolfson Institute for Biomedical Research, University College London, London, UK.

School of Basic Medical Sciences, Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.

出版信息

Dev Neurobiol. 2021 Nov;81(8):975-984. doi: 10.1002/dneu.22854. Epub 2021 Oct 24.

DOI:10.1002/dneu.22854
PMID:34601807
Abstract

Oligodendrocytes (OLs) continue to be generated from OL precursors (OPs) in the adult mammalian brain. Adult-born OLs are believed to contribute to neural plasticity, learning and memory through a process of "adaptive myelination," but how adult OL generation and adaptive myelination are regulated remains unclear. Here, we report that the glia-specific G protein-coupled receptor 37-like 1 (GPR37L1) is expressed in subsets of OPs and newly formed immature OLs in adult mouse brain. We found that OP proliferation and differentiation are inhibited in the corpus callosum of adult Gpr37l1 knockout mice, leading to a reduction in the number of adult-born OLs. Our data raise the possibility that GPR37L1 is mechanistically involved in adult OL generation and adaptive myelination, and suggest that GPR37L1 might be a useful functional marker of OPs that are committed to OL differentiation.

摘要

少突胶质细胞(OLs)在成年哺乳动物大脑中继续由 OL 前体细胞(OPs)产生。人们认为,新生的 OL 通过“适应性髓鞘形成”有助于神经可塑性、学习和记忆,但成年 OL 的产生和适应性髓鞘形成是如何调节的仍不清楚。在这里,我们报告在成年小鼠大脑中,胶质细胞特异性 G 蛋白偶联受体 37 样 1(GPR37L1)在 OP 亚群和新形成的未成熟 OL 中表达。我们发现,成年 Gpr37l1 基因敲除小鼠的胼胝体中 OP 增殖和分化受到抑制,导致新生 OL 数量减少。我们的数据提出了 GPR37L1 可能在成年 OL 产生和适应性髓鞘形成中具有机制作用的可能性,并表明 GPR37L1 可能是一种有用的功能性 OP 标志物,其可用于促进 OL 分化。

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