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.

中文翻译：

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EphA2 过表达减少 H2O2 诱导的晶状体上皮细胞损伤。

年龄相关性白内障 (ARC) 是一种发生在中老年的渐进性晶状体混浊。据报道，Eph 受体酪氨酸激酶 A2 型 (EphA2) 与 ARC 相关。这项工作旨在研究 EphA2 在 ARC 中的分子机制。我们用不同浓度的 H2O2 处理人晶状体上皮细胞 (SRA01/04) 以诱导晶状体上皮细胞损伤。然后，我们发现 H2O2 处理显着抑制了细胞活力并增强了 SRA01/04 细胞中 EphA2 的表达。H2O2 处理抑制了细胞活力并提高了 SRA01/04 细胞中活性氧 (ROS) 的水平，这部分被 EphA2 上调所消除。此外，EphA2 过表达减少了 H2O2 诱导的 SRA01/04 细胞凋亡。EphA2 上调导致 Bcl-2 上调，并抑制 H2O2 处理后 SRA01/04 细胞中 Bax 和 Cleaved-caspase-3 的表达。总之，我们的数据证实，在 H2O2 处理的 SRA01/04 细胞中，EphA2 过表达增强了细胞活力并抑制了细胞凋亡，从而减少了 H2O2 诱导的晶状体上皮细胞损伤。因此，这项工作为 EphA2 在 ARC 中的机制提供了新的见解。