MiR-23b-3p regulates apoptosis and autophagy via suppressing SIRT1 in lens epithelial cells.

Abstract

Age-related cataract is one of the prior causes of blindness and the incidence rates of cataract are even rising. Oxidative stress plays an important role in the pathogenesis of cataracts. Under oxidative stress, lens epithelial cell (LEC cell) apoptosis is activated, which might lead to the opacity of the lens and accelerate the progression of cataract development. Meanwhile, autophagy is also active to face oxidative stress. miRNAs have been reported to involve cataract. However, the underlying mechanism is not clear. The present study aimed to investigate the regulatory effect of miR23b-3p on apoptosis and autophagy in LEC cells under oxidative stress. The expression levels of miR-23b-3p were examined in age-related cataract tissues and LEC cells treated with hydrogen peroxide, showing that miR23b-3p expression levels were upregulated. Knockdown of miR23b-3p expression in LEC cells brought about apoptosis significantly decreased while autophagy significantly increased during hydrogen peroxide. We predicted microRNA miRNA-23b-3p might participate in regulating silent information regulator 1 (SIRT1) by bioinformatics database of TargetScan. Luciferase reporter assays confirmed that miRNA-23b-p could suppress SIRT1 expression by binding its 3'UTR. In addition, overexpression or knockdown of miR-23b-3p could decrease or increase SIRT1 expression, which indicated that Mir-23b-3p could suppress SIRT1 expression. In addition, enhanced SIRT1 could attenuate the regulation of cell apoptosis and autophagy induced by overexpression of miR-23b-3p. Taken together, our findings revealed that miR-23b-3p regulated apoptosis and autophagy via suppressing SIRT1 in LEC cell under oxidative stress, which could provide new ideas for clinical treatment of cataract.