Diabetic retinopathy (DR) is a common complication of diabetes mellitus (DM), which results in vision loss. This study explored the role of miR-126 in high-glucose-induced human retinal endothelial cells (HRECs) and its underlying molecular mechanisms. The results showed that the expression levels of miR-126 and interleukin-17A (IL-17A) in high-glucose-induced HRECs were 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 promoting the 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. This indicates that miR-126 enhances proliferation and inhibits apoptosis in high-glucose-induced HRECs by activating the PI3K-AKT pathway, increasing survivin levels, and decreasing Bax and caspase-3 expression by targeting IL-17A, suggesting that miR-126 could be a novel target for preventing DR.

中文翻译：

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MiR-126靶向IL-17A以增强高糖诱导的人视网膜内皮细胞的增殖并抑制细胞凋亡。

糖尿病性视网膜病（DR）是糖尿病（DM）的常见并发症，会导致视力丧失。这项研究探讨了miR-126在高糖诱导的人视网膜内皮细胞（HRECs）中的作用及其潜在的分子机制。结果表明，高糖诱导的HRECs中miR-126和白介素17A（IL-17A）的表达水平分别下调和上调。在功能上，miR-126的过表达促进了高葡萄糖诱导的HRECs的增殖并抑制了细胞凋亡，而IL-17A逆转了miR-126诱导的作用。然而，IL-17A的过表达抑制增殖并诱导凋亡，而敲低IL-17A则加速增殖并抑制凋亡。此外，miR-126抑制IL-17A，Bax和caspase-3的表达，同时促进survivin的表达以及PI3K和AKT的磷酸化；IL-17A的恢复挽救了这些影响。此外，IL-17A被鉴定为miR-126的靶标。这表明miR-126通过激活PI3K-AKT途径，增加survivin水平以及通过靶向IL-17A降低Bax和caspase-3表达来增强高糖诱导的HREC中的增殖并抑制其凋亡，这表明miR-126可以成为预防DR的新目标。