EphA2 overexpression reduces H2O2-induced
damage of lens epithelial cells |
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| Authors: | Qingshan Ji Jing Liu Guifang Wang Lian Liu Jingxiang Zhong |
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| Institution: | 1.University of Science and Technology of China, Affiliated First Hospital of USTC, Division of Life Sciences and Medicine, Department of Ophthalmology, Hefei, China.; 2.Ophthalmic Hospital of Wuhu, Department of Ophthalmology, Wuhu, China.; 3.Loudi Central Hospital of Hunan, Department of Ophthalmology, China.; 4.Affiliated First Hospital of Jinan University, Department of Ophthalmology, Guangzhou, China. |
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| Abstract: | 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. |
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| Keywords: | EphA2 cell viability apoptosis ROS age-related cataract |
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