| Literature DB >> 28728023 |
Xiao-Ling Hu1, Guo Chen2, Sanguo Zhang2, Jiangli Zheng3, Jun Wu3, Qing-Ran Bai4, Yue Wang5, Ji Li3, Huanhuan Wang2, Han Feng3, Jia Li6, Xicai Sun3, Qijun Xia7, Fan Yang8, Jing Hang3, Chang Qi3, Timothy N Phoenix5, Sally Temple5, Qin Shen9.
Abstract
During development, neural stem cells (NSCs) undergo transitions from neuroepithelial cells to radial glial cells (RGCs), and later, a subpopulation of slowly dividing RGCs gives rise to the quiescent adult NSCs that populate the ventricular-subventricular zone (V-SVZ). Here we show that VCAM1, a transmembrane protein previously found in quiescent adult NSCs, is expressed by a subpopulation of embryonic RGCs, in a temporal and region-specific manner. Loss of VCAM1 reduced the number of active embryonic RGCs by stimulating their premature neuronal differentiation while preventing quiescence in the slowly dividing RGCs. This in turn diminished the embryonic origin of postnatal NSCs, resulting in loss of adult NSCs and defective V-SVZ regeneration. VCAM1 affects the NSC fate by signaling through its intracellular domain to regulate β-catenin signaling in a context-dependent manner. Our findings provide new insight on how stem cells in the embryo are preserved to meet the need for growth and regeneration.Entities:
Keywords: VCAM1; embryonic origin; forebrain development; neural stem cells; neurogenesis; pre-B1 cells; regeneration; self-renewal; stem cell maintenance
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Year: 2017 PMID: 28728023 DOI: 10.1016/j.neuron.2017.06.047
Source DB: PubMed Journal: Neuron ISSN: 0896-6273 Impact factor: 17.173