EphA2 overexpression reduces H(2)O(2)-induced damage of lens epithelial cells

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 H(2)O(2) to induce lens epithelial cell damage. Then, we found that H(2)O(2) treatment significantly suppressed cell viability and enhanced the expression of EphA2 in the SRA01/04 cells. H(2)O(2) 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 H(2)O(2)-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 H(2)O(2) treatment. In conclusion, our data confirm that EphA2 overexpression enhances cell viability and inhibits apoptosis in the H(2)O(2)-treated SRA01/04 cells, thereby reducing H(2)O(2)-induced damage of lens epithelial cells. Thus, this work provides new insights into the mechanism of EphA2 in ARC.