文献类型：期刊文献

英文题名：CircMED12L Protects Against Hydrogen Peroxide-induced Apoptotic and Oxidative Injury in Human Lens Epithelial Cells by miR-34a-5p/ALCAM axis

作者：Wu, Baohua[1];Sun, Yan[2,3];Hou, Jingmei[1,2]

第一作者：Wu, Baohua

通信作者：Sun, Y[1]

机构：[1]Lanzhou Purui Ophthalmol Hosp, Dept Ophthalmol, Lanzhou, Peoples R China;[2]Gansu Rehabil Ctr Hosp, Dept Ophthalmol, 53 Dingxi Rd, Lanzhou 730000, Peoples R China;[3]Gansu Univ Chinese Med, Clin Sch Tradit Chinese, Lanzhou, Peoples R China

第一机构：Lanzhou Purui Ophthalmol Hosp, Dept Ophthalmol, Lanzhou, Peoples R China

通信机构：[1]corresponding author), Gansu Rehabil Ctr Hosp, Dept Ophthalmol, 53 Dingxi Rd, Lanzhou 730000, Peoples R China.

年份：2022

卷号：47

期号：12

起止页码：1631

外文期刊名：CURRENT EYE RESEARCH

收录：;Scopus(收录号：2-s2.0-85140389718);WOS:【SCI-EXPANDED(收录号:WOS:000871357300001)】；

基金：This study was supported by the Key R&D Plan of Gansu Provincial Department of Science and Technology (20YF8FA111), Lanzhou Talent Innovation and Entrepreneurship Project (2019-RC-39; 2020-RC-91)

语种：英文

外文关键词：CircMED12L; miR-34a-5p; ALCAM; age-related cataract; oxidative stress

摘要：Purpose Cataract is the leading cause of visual impairment and reversible blindness. Despite advances in surgical removal of cataracts, cataract continues to be a leading public-health issue due to the complications after surgery. Circular RNAs (circRNAs) have been showed to be implicated in the pathophysiology of age-related cataract (ARC). Herein, this work elucidated the role and mechanism of circMED12L in the process of ARC. Methods Human lens epithelial cells (HLECs) were exposed to hydrogen peroxide (H2O2) in experimental groups. Levels of genes and proteins were measured by qRT-PCR and western blotting. Cell growth was evaluated by Cell Counting Kit-8 (CCK-8) assay and flow cytometry, respectively. The oxidative stress was assessed by detecting the activity of malondialdehyde, catalase, and superoxide dismutase. The interaction between miR-34a-5p and circMED12L or ALCAM (activated leukocyte cell adhesion molecule) was validated using dual-luciferase reporter and RNA immunoprecipitation assays. Results CircMED12L expression was lower in the lens epithelium of ARC patients and H2O2-induced HLECs compared with the normal individuals and untreated cells. Functionally, forced expression of circMED12L could alleviate H2O2-induced viability inhibition, as well as apoptotic and oxidative injury in HLECs. Mechanistically, circMED12L/miR-34a-5p/ALCAM constituted a feedback loop in HLECs. MiR-34a-5p was increased, while ALCAM was decreased in ARC patients and H2O2-induced HLECs. High expression of miR-34a-5p reversed the protective effects of circMED12L on HLECs under H2O2 treatment. Besides, inhibition of miR-34a-5p could repress H2O2-induced apoptotic and oxidative injury in HLECs, which were abolished by subsequent ALCAM knockdown. Conclusion Overexpression of circMED12L could protect against H2O2-induced apoptosis and oxidative stress in HLECs by miR-34a-5p/ALCAM axis.