Journal
BIOSCIENCE REPORTS
Volume 40, Issue -, Pages -Publisher
PORTLAND PRESS LTD
DOI: 10.1042/BSR20201545
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Funding
- Special Grant for High-level Personnel of Yunnan Province [D-201619]
- Association Foundation Program of Yunnan Provincial Science and Technology Department and Kunming Medical University [2019FE001(-169)]
- Young and Middle-aged Technical Academic Leaders Training Project in Yunnan Province [202005AC160021]
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Increasing evidence has shown that microRNAs (miRNAs) play an important role in the pathogenesis of diabetic retinopathy (DR). However, the role and mechanism of miRNA in regulating high glucose (HG)-induced ARPE-19 cell injury are still not well understood. The present study aimed to investigate the effects of miR-200a-3p on DR progression and reveal the underlying mechanisms of their effects. In the present study, we observed that miR-200a-3p was significantly decreased, while transforming growth factor-beta 2 (TGF-beta 2) expression was up-regulated in ARPE-19 cells treated with HG and retina tissues of DR rats. Subsequently, overexpression of miR-200a-3p significantly promoted cell proliferation, reduced apoptosis, as well as inhibited the levels of inflammatory cytokines secreted, matrix metalloprotease 2/9 (MMP2/9), and vascular endothelial growth factor (VEGF) in HG-injured ARPE-19 cells. Moreover, miR-200a-3p was proved to target TGF-beta 2 mRNA by binding to its 3' untranslated region (3'UTR) using a luciferase reporter assay. Mechanistically, overexpression of miR-200a-3p reduced HG-induced ARPE-19 cell injury and reduced inflammatory cytokines secreted, as well as down-regulated the expression of VEGF via inactivation of the TGF-beta 2/Smad pathway in vitro. In vivo experiments, up-regulation of miR-200a-3p ameliorated retinal neovascularization and inflammation of DR rats. In conclusion, our findings demonstrated that miR-200a-3p-elevated prevented DR progression by blocking the TGF-beta 2/Smad pathway, providing a new therapeutic biomarker for DR treatment in the clinic.
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