Research Paper|Volume 13, Issue 12|pp 16062—16071

PirB functions as an intrinsic suppressor in hippocampal neural stem cells

Baiyang Liu^1,², Wenjing Cheng¹, Dating Cheng³, Jun Pu³, Zhi Nie^1,^2,³, Cuifeng Xia³, Yongbin Chen^1,⁴, Cuiping Yang¹

¹Key Laboratory of Animal Models and Human Disease Mechanisms of Chinese Academy of Sciences & Yunnan Province, Kunming Institute of Zoology, Kunming, Yunnan 650223, China
²Kunming College of Life Science, University of Chinese Academy of Sciences, Beijing 100049, China
³Kunming Medical University, Kunming, Yunnan 650500, China
⁴Center for Excellence in Animal Evolution and Genetics, Chinese Academy of Sciences, Kunming, Yunnan 650223, China

* Equal contribution

Received: February 19, 2021Accepted: May 18, 2021Published: June 13, 2021

https://doi.org/10.18632/aging.203134

Copyright: © 2021 Liu et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

Neural stem cells play pivotal roles during prenatal development and throughout life. Here, we report that Paired immunoglobulin-like receptor B (PirB) functions as a suppressor during brain neurogenesis in the adult mouse. PirB expression increased with age during development, and its deficiency promoted neural stem cell proliferation and differentiation in vivo and in vitro. Furthermore, we detected an increase in Type 1 neural stem cells in PirB-deficient mice compared to their wild-type littermates. PirB deficiency promoted stemness marker gene expression of Sox2 and KLF4 by activating Akt1 phosphorylation. These findings suggest that PirB inhibits the self-renewal and differentiation capacities of neural stem cells. Thus, PirB may have the potential to serve as a therapeutic target for treatment of reduced neurogenesis in adults due to aging or other pathological conditions.