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

The EMBO Journal, 2020 · DOI: 10.15252/embj.2019101679 · Published: February 3, 2020

Simple Explanation

Adult neural stem cells (NSCs) reside in specialized niches, which hold a balanced number of NSCs, their progeny, and other cells. 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). Thus, ependyma-derived CCN1 restricts NSC expansion in the adult brain to maintain the proper niche capacity of the V-SVZ.

Study Duration

Not specified

Participants

Mice

Evidence Level

Not specified

Key Findings

1
CCN1 is specifically expressed in ependymal cells in the adult V-SVZ.
2
CCN1 negatively regulates niche capacity and B1 cell number in the adult V-SVZ.
3
Loss of CCN1 transiently enhanced NSC proliferation and reduced differentiation.

Research Summary

Here we show that the matricellular protein CCN1, which is selectively expressed in the ependymal cells, constrains the niche capacity, maintaining a balanced number of NSCs in the adult V-SVZ. Our results present a niche regulatory strategy by which ependymal factor CCN1 controls the activation of NSCs and subsequent accommodation and maintenance of qNSCs in the apical niche surface of the V-SVZ. Our study has identified a novel ependyma-specific niche factor and revealed that CCN1 imposes a constraining effect on V-SVZ niche capacity and the size of NSC pool, implying the complexity of stem cell niche control.

Practical Implications

Niche Capacity Regulation

Ependymal-derived CCN1 restricts NSC expansion in the adult brain to maintain proper V-SVZ niche capacity.

Therapeutic Potential

Understanding CCN1's role could lead to targeted therapies for neurological disorders by manipulating NSC pool size.

Aging Research

The study provides insights into how the V-SVZ niche changes with age and how CCN1 contributes to NSC maintenance over time.

Study Limitations

1
The study focuses primarily on mice, and the findings may not directly translate to humans.
2
The precise molecular mechanisms by which CCN1 regulates NSC fate remain unclear.
3
The long-term consequences of CCN1 deficiency on overall brain function were not fully explored.

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