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SDF-1/CXCR4信号通路维持小鼠神经干细胞/祖细胞的干性特征。

SDF-1/CXCR4 Signaling Maintains Stemness Signature in Mouse Neural Stem/Progenitor Cells.

作者信息

Ho Shih-Yin, Ling Thai-Yen, Lin Hsing-Yu, Liou Jeffrey Tsai-Jui, Liu Fei-Chih, Chen I-Chun, Lee Sue-Wei, Hsu Yu, Lai Dar-Ming, Liou Horng-Huei

机构信息

Department of Neurology, National Taiwan University Hospital, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.

Department of Pharmacology, College of Medicine, National Taiwan University, Taipei 10051, Taiwan.

出版信息

Stem Cells Int. 2017;2017:2493752. doi: 10.1155/2017/2493752. Epub 2017 Mar 20.

DOI:10.1155/2017/2493752
PMID:28408934
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5376953/
Abstract

SDF-1 and its primary receptor, CXCR4, are highly expressed in the embryonic central nervous system (CNS) and play a crucial role in brain architecture. Loss of SDF-1/CXCR4 signaling causes abnormal development of neural stem/progenitor cells (NSCs/NPCs) in the cerebellum, hippocampus, and cortex. However, the mechanism of SDF-1/CXCR4 axis in NSCs/NPCs regulation remains unknown. In this study, we found that elimination of SDF-1/CXCR4 transduction caused NSCs/NPCs to lose their stemness characteristics and to encounter neurogenic differentiation. Moreover, Notch and RE1 silencing transcription factor (REST) both play an essential role in NSCs/NPCs maintenance and neuronal differentiation and were dramatically downregulated following SDF-1/CXCR4 cascade inhibition. Finally, we demonstrated that the expression of achaete-scute homolog 1 (Ascl1), a proneural gene, and p27, an antiproliferative gene, were significantly increased after genetic elimination of SDF-1 alleles. Our results support that the loss of functional SDF-1/CXCR4 signaling pathway in NSCs/NPCs induces exit of cell cycle and promotes premature neural differentiation.

摘要

基质细胞衍生因子-1（SDF-1）及其主要受体CXC趋化因子受体4（CXCR4）在胚胎中枢神经系统（CNS）中高表达，并在脑结构中发挥关键作用。SDF-1/CXCR4信号缺失会导致小脑、海马体和皮质中的神经干/祖细胞（NSCs/NPCs）发育异常。然而，SDF-1/CXCR4轴在NSCs/NPCs调控中的机制仍不清楚。在本研究中，我们发现消除SDF-1/CXCR4信号转导会导致NSCs/NPCs失去其干性特征并发生神经源性分化。此外，Notch和RE1沉默转录因子（REST）在NSCs/NPCs维持和神经元分化中均起重要作用，并且在SDF-1/CXCR4级联抑制后显著下调。最后，我们证明，在基因消除SDF-1等位基因后，神经母细胞基因achaete-scute同源物1（Ascl1）和抗增殖基因p27的表达显著增加。我们的结果支持，NSCs/NPCs中功能性SDF-1/CXCR4信号通路的缺失会诱导细胞周期退出并促进神经细胞过早分化。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/92c19aba0e77/SCI2017-2493752.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/268810f9c784/SCI2017-2493752.001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/8a072f6c0841/SCI2017-2493752.005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/92c19aba0e77/SCI2017-2493752.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/268810f9c784/SCI2017-2493752.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/92821e3111bf/SCI2017-2493752.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/fe45f10fc615/SCI2017-2493752.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/d646f24974ab/SCI2017-2493752.004.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/c880aab9f70a/SCI2017-2493752.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/be6f/5376953/92c19aba0e77/SCI2017-2493752.007.jpg

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