MiR-24-p53 pathway evoked by oxidative stress promotes lens epithelial cell apoptosis in age-related cataracts

Abstract

MicroRNA-24 (miR-24) serves an important role in cell proliferation, migration and inflammation in various types of disease. In the present-study, the biological function and molecular mechanism of miR-24 was investigated in association with the progression of age-associated cataracts. To the best of our knowledge the present-study is the first to report that the expression of miR-24 was significantly increased in human anterior lens capsules affected by age-associated cataracts as well as lens epithelial cells (LECs) exposed to oxidative stress. Overexpression of miR-24 induced p53 expression and p53 was verified as a direct target of miR-24. Overexpression of miR-24 enhanced LEC death by directly targeting p53. The present-study revealed that oxidative stress induced the upregulation of miR-24 and enhanced LEC death by directly targeting p53. These results suggest that the miR-24-p53 signaling pathway is involved in a novel mechanism of age-associated cataractogenesis and miR-24 may be a useful therapeutic target for age-associated cataracts.