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转录因子 7 样 2 促进少突胶质细胞分化和髓鞘再生。

Transcription factor 7 like 2 promotes oligodendrocyte differentiation and remyelination.

机构信息

Department of Neurology, Renmin Hospital of Wuhan University, Wuhan, Hubei 430060, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):1864-1870. doi: 10.3892/mmr.2017.6843. Epub 2017 Jun 22.

Abstract

Transcription factor 7 like 2 (TCF7L2, also termed TCF4), is a Wnt effector induced transiently in the oligodendroglial lineage. The current well accepted hypothesis is that TCF7L2 inhibits oligodendrocyte differentiation and remyelination through canonical Wnt/β‑catenin signaling. However, recent studies indicated that TCF7L2 activity is required during oligodendrocyte differentiation and remyelination. In order to clarify this, in situ hybridization, immunofluorescence and western blot analysis using in vivo TCF7L2 conditional knockout mice, were performed and it was found that TCF7L2 promotes oligodendrocyte differentiation during myelin formation and remyelination. Furthermore, it was established that TCF7L2 does not affect oligodendrocyte precursor cells during remyelination. These data are of important clinical significance to develop novel therapeutic targets to overcome multiple sclerosis and other demyelinating diseases.

摘要

转录因子 7 样蛋白 2(TCF7L2,也称为 TCF4)是一种在少突胶质细胞谱系中瞬时诱导的 Wnt 效应物。目前公认的假设是,TCF7L2 通过经典 Wnt/β-catenin 信号通路抑制少突胶质细胞分化和髓鞘再生。然而,最近的研究表明,TCF7L2 活性在少突胶质细胞分化和髓鞘再生过程中是必需的。为了阐明这一点,使用体内 TCF7L2 条件性敲除小鼠进行了原位杂交、免疫荧光和 Western blot 分析,结果发现 TCF7L2 促进髓鞘形成和髓鞘再生过程中的少突胶质细胞分化。此外,还确定 TCF7L2 在髓鞘再形成过程中不影响少突胶质前体细胞。这些数据对于开发新的治疗靶点以克服多发性硬化症和其他脱髓鞘疾病具有重要的临床意义。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/a833/5562062/a9d69da3d0a7/MMR-16-02-1864-g00.jpg

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