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.

中文翻译：

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室管膜表达的CCN1限制了成人心室-室下区神经干细胞池的大小。

成年神经干细胞（NSC）驻留在专门的壁ches中，这些壁hold拥有均衡数量的NSC，它们的后代和其他细胞。目前尚不清楚如何调节利基能力以包含特定数量的NSC。在这里，我们显示，室管膜源性基质细胞蛋白CCN1（细胞通讯网络因子1）负调节成年心室－室下区（V-SVZ）的生态位容量和NSC数量。成年室管膜特异性Ccn1缺失会暂时增强小鼠NSC增殖并减少神经元分化，从而增加NSC和NSC单位的数量。尽管在Ccn1基因敲除小鼠中看到的NSC增殖和神经发生最终恢复正常，但扩大的NSC库仍保留在V-SVZ中直至老年。EGFR信号转导的抑制阻止了CCN1缺陷小鼠中NSC群体的扩展。因此，室管膜源性CCN1限制了成年大脑中NSC的扩增，以维持V-SVZ的适当小生境能力。