Aging
Navigate
Submit an Article
Research Paper|Volume 14, Issue 15|pp 6128—6148

MAB21L1 promotes survival of lens epithelial cells through control of αB-crystallin and ATR/CHK1/p53 pathway

Yuan Xiao1,2, Jia-Wen Xiang2, Qian Gao1,2, Yue-Yue Bai1,2, Zhao-Xia Huang3, Xiao-Hui Hu1, Ling Wang4, David Wan-Cheng Li1,2
  • 1College of Life Sciences, Hunan Normal University, Changsha 410080, Hunan, China
  • 2The State Key Laboratory of Ophthalmology, Zhongshan Ophthalmic Center, Sun Yat-Sen University, Tianhe, Guangzhou 510230, Guangdong, China
  • 3Department of Basic Medicine, Guizhou University of Traditional Chinese Medicine, Guiyang 121212, Guizhou, China
  • 4The Academician Work Station, Changsha Medical University, Changsha 410219, Hunan, China
* Co-first author
Received: March 1, 2022Accepted: July 25, 2022Published: August 10, 2022
https://doi.org/10.18632/aging.204203

Copyright: © 2022 Xiao 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

The male abnormal gene family 21 (mab21), was initially identified in C. elegans. Since its identification, studies from different groups have shown that it regulates development of ocular tissues, brain, heart and liver. However, its functional mechanism remains largely unknown. Here, we demonstrate that Mab21L1 promotes survival of lens epithelial cells. Mechanistically, Mab21L1 upregulates expression of αB-crystallin. Moreover, our results show that αB-crystallin prevents stress-induced phosphorylation of p53 at S-20 and S-37 through abrogating the activation of the upstream kinases, ATR and CHK1. As a result of suppressing p53 activity by αB-crystallin, Mab21L1 downregulates expression of Bak but upregulates Mcl-1 during stress insult. Taken together, our results demonstrate that Mab21L1 promotes survival of lens epithelial cells through upregulation of αB-crystallin to suppress ATR/CHK1/p53 pathway.