MiR-126 targets IL-17A to enhance proliferation and inhibit apoptosis in high-glucose-induced human retinal endothelial cells
| Autor: | Xiujuan Chen, Cuihong Guan, Li Li, Xuequn Yu, Ting Guo, Guoping Cao, Fang Li, Xinxiang Li, Liping Miao |
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| Rok vydání: | 2020 |
| Předmět: |
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 |
| Zdroj: | Biochemistry and Cell Biology. 98:277-283 |
| ISSN: | 1208-6002 0829-8211 |
| DOI: | 10.1139/bcb-2019-0174 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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