1. MiR-126 targets IL-17A to enhance proliferation and inhibit apoptosis in high-glucose-induced human retinal endothelial cells
- Author
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Xiujuan Chen, Cuihong Guan, Li Li, Xuequn Yu, Ting Guo, Guoping Cao, Fang Li, Xinxiang Li, and Liping Miao
- Subjects
0301 basic medicine ,Survivin ,Apoptosis ,Biochemistry ,Retina ,Phosphatidylinositol 3-Kinases ,03 medical and health sciences ,chemistry.chemical_compound ,0302 clinical medicine ,Diabetes mellitus ,medicine ,Humans ,Phosphorylation ,Molecular Biology ,Cell Proliferation ,bcl-2-Associated X Protein ,Binding Sites ,Diabetic Retinopathy ,business.industry ,Gene Expression Profiling ,Interleukin-17 ,Endothelial Cells ,Retinal ,Cell Biology ,Diabetic retinopathy ,medicine.disease ,MicroRNAs ,Glucose ,030104 developmental biology ,Gene Expression Regulation ,chemistry ,030220 oncology & carcinogenesis ,High glucose ,Cancer research ,Complication ,business ,Proto-Oncogene Proteins c-akt ,Signal Transduction - Abstract
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.
- Published
- 2020