2020 journal article

Ependyma-expressed CCN1 restricts the size of the neural stem cell pool in the adult ventricular-subventricular zone

EMBO JOURNAL, 39(5).

By: J. Wu *, W. Tian*, Y. Liu *, H. Wan*, J. Zheng *, X. Wang *, H. Pan *, J. Li * ...

author keywords: CCN1; EGFR; ependymal cells; neural stem cells; niche
MeSH headings : Adult Stem Cells / physiology; Animals; Brain; Cysteine-Rich Protein 61 / genetics; Cysteine-Rich Protein 61 / metabolism; Ependyma / cytology; Ependyma / metabolism; ErbB Receptors / genetics; ErbB Receptors / metabolism; Female; Male; Mice; Mice, Inbred C57BL; Mice, Knockout; Neural Stem Cells / cytology; Neural Stem Cells / metabolism; Neurogenesis / physiology; Signal Transduction
TL;DR: It is shown that ependyma‐derived matricellular protein CCN1 (cellular communication network factor 1) negatively regulates niche capacity and NSC number in the adult ventricular–subventricular zone (V‐SVZ) of the adult brain to maintain the proper niche capacity of the V‐VZ. (via Semantic Scholar)
UN Sustainable Development Goal Categories
Source: Web Of Science
Added: February 17, 2020

Adult neural stem cells (NSCs) reside in specialized niches, which hold a balanced number of NSCs, their progeny, and other cells. How niche capacity is regulated to contain a specific number of NSCs remains unclear. Here, we show that ependyma‐derived matricellular protein CCN1 (cellular communication network factor 1) negatively regulates niche capacity and NSC number in the adult ventricular–subventricular zone (V‐SVZ). Adult ependyma‐specific deletion of Ccn1 transiently enhanced NSC proliferation and reduced neuronal differentiation in mice, increasing the numbers of NSCs and NSC units. Although proliferation of NSCs and neurogenesis seen in Ccn1 knockout mice eventually returned to normal, the expanded NSC pool was maintained in the V‐SVZ until old age. Inhibition of EGFR signaling prevented expansion of the NSC population observed in CCN1 deficient mice. Thus, ependyma‐derived CCN1 restricts NSC expansion in the adult brain to maintain the proper niche capacity of the V‐SVZ.