EphA2 overexpression reduces H2O2-induced damage of lens epithelial cells Cellular, Molecular and Developmental Genetics

• Published in: Genetics and molecular biology Vol. 44; no. 3; p. 1
• Main Authors: Ji, Qingshan, Liu, Jing, Wang, Guifang, Liu, Lian, Zhong, Jingxiang
• Format: Journal Article
• Language: English
• Published: Ribeirao Preto Sociedade Brasileira de Genetica 01.01.2021
• Subjects: Apoptosis; Bcl-2 protein; Caspase-3; Cataracts; Cell viability; Damage; Developmental genetics; EphA2 protein; Epithelial cells; Epithelium; Genetics; Hydrogen peroxide; Lenses; Reactive oxygen species
• DOI: 10.1590/1678-4685-GMB-2020-0414
• ISSN: 1415-4757

Age-related cataract (ARC) is a progressive lens opacification that occurs from middle to old age. Eph-receptor tyrosinekinase-type A2 (EphA2) has been reported to be associated with ARC. This work aims to investigate the molecular mechanism of EphA2 in ARC. We treated human lens epithelial cells (SRA01/04) with different concentration of H2O2 to induce lens epithelial cell damage. Then, we found that H2O2 treatment significantly suppressed cell viability and enhanced the expression of EphA2 in the SRA01/04 cells. H2O2 treatment repressed cell viability and enhanced the levels of reactive oxygen species (ROS) in SRA01/04 cells, which was partly abolished by EphA2 up-regulation. Moreover, EphA2 overexpression reduced H2O2-induced apoptosis of SRA01/04 cells. EphA2 up-regulation caused an up-regulation of Bcl-2, and repressed the expression of Bax and Cleaved-caspase-3 in the SRA01/04 cells following H2O2 treatment. In conclusion, our data confirm that EphA2 overexpression enhances cell viability and inhibits apoptosis in the H2O2-treated SRA01/04 cells, thereby reducing H2O2-induced damage of lens epithelial cells. Thus, this work provides new insights into the mechanism of EphA2 in ARC.