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.