miR-17-5p regulates the proliferation and apoptosis of human trabecular meshwork cells by targeting phosphatase and tensin homolog

Glaucoma is one of the leading causes of blindness. Previous studies have indicated that the oxidative stress-induced apoptosis of trabecular meshwork cells (TMCs) may serve a key role in the pathogenesis of glaucoma, and that micro RNA(miR)-17-5p may be involved in this process. However, the specific mechanisms require further investigation. The aim of the present study was to investigate the effects of miR-17-5p on the proliferation and apoptosis of human TMCs (HTMCs) in response to oxidative stress. It was observed that exposure to H(2)O(2) induced a significant decrease in the proliferation and a marked increase in the apoptosis of HTMCs. H(2)O(2) exposure also suppressed the expression of miR-17-5p and promoted the expression of phosphatase and tensin homolog (PTEN). Furthermore, transient overexpression of miR-17-5p induced a significant increase in the proliferation and a significant decrease in the apoptosis of HTMCs by affecting the expression of PTEN, and the apoptosis-related proteins B-cell lymphoma-associated X protein (Bax), B-cell lymphoma-extra large (Bcl-xL) and B-cell lymphoma-2 (Bcl-2). However, knockdown of miR-17-5p demonstrated the opposite results. The results of a dual luciferase reporter assay demonstrated that PTEN may be a direct target of miR-17-5p. In conclusion, miR-17-5p was downregulated in HTMCs under oxidative conditions, and miR-17-5p may regulate the apoptosis of HTMCs by targeting PTEN. These results provide a novel theoretical basis and potential therapeutic target for the treatment of glaucoma.