Circular RNA circGlis3 protects against islet β-cell dysfunction and apoptosis in obesity

Yue Liu, Yue Yang, Chenying Xu, Jianxing Liu, Jiale Chen, Guoqing Li, Bin Huang, Yi Pan, Yanfeng Zhang, Qiong Wei, Stephen J. Pandol, Fangfang Zhang (), Ling Li () and Liang Jin ()
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Yue Liu: School of life Science and Technology, China Pharmaceutical University
Yue Yang: School of life Science and Technology, China Pharmaceutical University
Chenying Xu: School of life Science and Technology, China Pharmaceutical University
Jianxing Liu: School of life Science and Technology, China Pharmaceutical University
Jiale Chen: School of life Science and Technology, China Pharmaceutical University
Guoqing Li: Zhongda Hospital, School of Medicine, Southeast University
Bin Huang: School of life Science and Technology, China Pharmaceutical University
Yi Pan: School of life Science and Technology, China Pharmaceutical University
Yanfeng Zhang: School of life Science and Technology, China Pharmaceutical University
Qiong Wei: Zhongda Hospital, School of Medicine, Southeast University
Stephen J. Pandol: Cedars-Sinai Medical Center
Fangfang Zhang: School of life Science and Technology, China Pharmaceutical University
Ling Li: Zhongda Hospital, School of Medicine, Southeast University
Liang Jin: School of life Science and Technology, China Pharmaceutical University

Nature Communications, 2023, vol. 14, issue 1, 1-19

Abstract: Abstract Pancreatic β-cell compensation is a major mechanism in delaying T2DM progression. Here we report the abnormal high expression of circGlis3 in islets of male mice with obesity and serum of people with obesity. Increasing circGlis3 is regulated by Quaking (QKI)-mediated splicing circularization. circGlis3 overexpression enhances insulin secretion and inhibits obesity-induced apoptosis in vitro and in vivo. Mechanistically, circGlis3 promotes insulin secretion by up-regulating NeuroD1 and Creb1 via sponging miR-124-3p and decreases apoptosis via interacting with the pro-apoptotic factor SCOTIN. The RNA binding protein FUS recruits circGlis3 and collectively assemble abnormal stable cytoplasmic stress granules (SG) in response to cellular stress. These findings highlight a physiological role for circRNAs in β-cell compensation and indicate that modulation of circGlis3 expression may represent a potential strategy to prevent β-cell dysfunction and apoptosis after obesity.

Date: 2023
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DOI: 10.1038/s41467-023-35998-z

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