MiR-126 targets IL-17A to enhance proliferation and inhibit apoptosis in high-glucose-induced human retinal endothelial cells

Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM), which results in vision loss. The present study aimed to explore the role of miR-126 in high-glucose-induced human retinal endothelial cells (HRECs) and its underlying molecular mechanism. The results showed that expression of miR-126 and interleukin-17A (IL-17A) in high-glucose-induced HRECs was downregulated and upregulated, respectively. Functionally, overexpression of miR-126 promoted proliferation and suppressed apoptosis in high-glucose-induced HRECs, while IL-17A reversed the effects induced by miR-126. However, overexpression of IL-17A inhibited the proliferation and induced apoptosis, while knockdown of IL-17A accelerated the proliferation and repressed apoptosis. In addition, miR-126 repressed the expression of IL-17A, Bax, and caspase-3,while promotingthe expression of survivin and phosphorylation of PI3K and AKT;restoration of IL-17A rescued these effects. Furthermore, IL-17A was identified as a target of miR-126. Altogether, miR-126 enhances proliferation and inhibits apoptosis in high-glucose-induced HRECs by activating the PI3K/AKT pathway, increasing survivinand decreasing Bax and caspase-3 expression by targeting IL-17A, suggesting that miR-126 may be a novel target for preventing DR.The accepted manuscript in pdf format is listed with the files at the bottom of this page. The presentation of the authors' names and (or) special characters in the title of the manuscript may differ slightly between what is listed on this page and what is listed in the pdf file of the accepted manuscript; that in the pdf file of the accepted manuscript is what was submitted by the author