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ErbB3 结合蛋白 1 通过调节 Bmp4 和 Ascl1 信号促进成年海马神经发生。

ErbB3 binding protein 1 contributes to adult hippocampal neurogenesis by modulating Bmp4 and Ascl1 signaling.

机构信息

Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419; Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon 16419, Korea.

Department of Molecular Cell Biology, Sungkyunkwan University School of Medicine, Suwon 16419; Single Cell Network Research Center, Sungkyunkwan University School of Medicine, Suwon 16419; Samsung Biomedical Research Institute, Samsung Medical Center, Seoul 06351, Korea.

出版信息

BMB Rep. 2024 Apr;57(4):182-187. doi: 10.5483/BMBRep.2023-0149.

DOI:10.5483/BMBRep.2023-0149
PMID:37817439
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11058358/
Abstract

Neural stem cells (NSCs) in the adult hippocampus divide infrequently; the endogenous molecules modulating adult hippocampal neurogenesis (AHN) remain largely unknown. Here, we show that ErbB3 binding protein 1 (Ebp1), which plays important roles in embryonic neurodevelopment, acts as an essential modulator of adult neurogenic factors. In vivo analysis of Ebp1 neuron depletion mice showed impaired AHN with a low number of hippocampal NSCs and neuroblasts. Ebp1 leads to transcriptional repression of Bmp4 and suppression of Ascl1 promoter methylation in the dentate gyrus of the adult hippocampus reflecting an unusually high level of Bmp4 and low Ascl1 level in neurons of Ebp1-deficient mice. Therefore, our findings suggests that Ebp1 could act as an endogenous modulator of the interplay between Bmp4 and Ascl1/Notch signaling, contributing to AHN. [BMB Reports 2024; 57(4): 182-187].

摘要

神经干细胞（NSCs）在成体海马中分裂不频繁；调节成体海马神经发生（AHN）的内源性分子在很大程度上尚不清楚。在这里，我们表明，在胚胎神经发育中发挥重要作用的 ErbB3 结合蛋白 1（Ebp1）是成年神经发生因子的必需调节剂。对 Ebp1 神经元耗竭小鼠的体内分析表明，AHN 受损，海马 NSCs 和神经前体细胞数量减少。Ebp1 导致 Bmp4 的转录抑制和成年海马齿状回中 Ascl1 启动子甲基化的抑制，反映出 Ebp1 缺陷型小鼠神经元中异常高的 Bmp4 和低水平的 Ascl1。因此，我们的研究结果表明，Ebp1 可以作为 Bmp4 和 Ascl1/Notch 信号之间相互作用的内源性调节剂，有助于 AHN。[BMB 报告 2024；57(4): 182-187]。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/d19e8f8b33dc/bmb-57-4-182-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/efc9e755b13e/bmb-57-4-182-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/0b41a296f734/bmb-57-4-182-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/db3aa9e00b38/bmb-57-4-182-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/d19e8f8b33dc/bmb-57-4-182-f4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/efc9e755b13e/bmb-57-4-182-f1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/0b41a296f734/bmb-57-4-182-f2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/db3aa9e00b38/bmb-57-4-182-f3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/fad6/11058358/d19e8f8b33dc/bmb-57-4-182-f4.jpg

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