AI Article Synopsis
- * Findings show that levels of phosphorylated MDM2 (p-MDM2) are lower in both human cataracts and aging cataract mice compared to normal samples.
- * The research indicates that MDM2 can regulate apoptosis in LECs and that its phosphorylation might be linked to treatments for ARC, suggesting potential for new clinical approaches.
Article Abstract
Lens epithelial cells (LECs) apoptosis induced by oxidative stress is a major factor in age-related-cataract (ARC) pathogenesis, but there are still many blind nodes in this progress. This study aimed to investigate the effects of MDM2 phosphorylation in ARC and HO-induced lens epithelial cells apoptosis. Our results confirmed that the levels of p-MDM2 (Ser166) and p-MDM2 (Ser186) in the anterior lens capsules of human cataracts were reduced compared to that in normal capsules. Similarly, in naturally aging cataract mice, the level of MDM2 phosphorylation also decreased. Oxidative stress-induced apoptosis model was constructed by cultivating HLE-B3 cells with 200 μM HO. It was confirmed that MDM2 could regulate lens epithelial cell apoptosis, and MDM2 inhibitors could partly inhibited AKT's role in suppressing apoptosis induced by HO. Besides, we examed the decreased level of p-AKT(Ser473) in apoptosis of lens epithelial cells and ARC. Our study revealed that MDM2 phosphorylation mediated HO-induced lens epithelial cells apoptosis and ARC, which could provide new ideas for the clinical treatment of ARC.
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| http://dx.doi.org/10.1016/j.bbrc.2020.05.060 | DOI Listing |
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