circ_0041795 Induces YAP1 Upregulation to Accelerate the Progression of Diabetic Retinopathy through Binding to miR-589-5p.

BACKGROUND

Circular RNAs (circRNAs) are involved in the pathogenesis of many diseases, and circ_0041795 was shown to promote the progression of diabetic retinopathy (DR). The aim of this study was to explore the molecular mechanism of circ_0041795 in DR.

METHODS

Human retinal pigment epithelial cells ARPE-19 were treated with high glucose (HG). circ_0041795, miR-589-5p, and Yes-associated protein 1 (YAP1) levels were measured by reverse transcription-quantitative polymerase chain reaction assay. Biological behaviors were examined by Cell Counting Kit-8 assay for cell viability, EdU assay for cell proliferation, flow cytometry for cell apoptosis, and enzyme-linked immunosorbent assay for cell inflammation. Oxidative stress was assessed via the commercial kits. Western blot was performed for analysis of protein expression. The molecular binding was assessed via dual-luciferase reporter assay and pull-down assay.

RESULTS

HG-induced inhibiting effects on cell viability and proliferation but promoting effects on cell apoptosis, inflammation, and oxidative stress were ameliorated by silence of circ_0041795. circ_0041795 was identified to act as a miR-589-5p sponge. The regulation of circ_0041795 in HG-induced cell injury was achieved by inhibiting miR-589-5p. miR-589-5p targeted YAP1 and relieved HG-induced cell dysfunction via downregulating YAP1. circ_0041795 sponged miR-589-5p to regulate YAP1 level and activated the NF-B pathway through the miR-589-5p/YAP1 axis.

CONCLUSION

All these results elucidated that circ_0041795 facilitated the development of DR by inducing miR-589-5p-mediated YAP1 upregulation.