Background
Diabetic retinopathy (DR) is a serious complication of diabetes. Numerous reports have validated that circular RNAs (circRNAs) participate in DR progression. This study aimed to elucidate the role and potential mechanism of circRNA zinc finger protein 532 (circZNF532) in DR.
Conclusion
circZNF532 facilitated HG-induced angiogenesis and inflammation in hRMECs via modulating the miR-1243/CARM1 pathway, suggesting that circZNF532 might be a potential biomarker for DR treatment.
Methods
The levels of circZNF532, miR-1243, and coactivator associated arginine methyltransferase 1 (CARM1) in DR patients and human retinal microvascular endothelial cells (hRMECs) were determined by quantitative real-time PCR and western blot. Colony formation assay, transwell assay, tube formation assay and enzyme-linked immunosorbent assay were used to assess the biological function of hRMECs. The binding relationship between miR-1243 and circZNF532/CARM1 was verified by dual-luciferase reporter and RNA immunoprecipitation assays.
Results
circZNF532 and CARM1 levels were increased, while miR-1243 level was reduced in DR patients and high glucose (HG)-stimulated hRMECs. In terms of mechanism, miR-1243 competitively bound to circZNF532 and CARM1. Down-regulation of circZNF532 restrained HG-induced hRMECs proliferation, migration, invasion, angiogenesis and inflammation via regulating miR-1243. In addition, miR-1243 inhibited HG-triggered hRMECs progression via targeting CARM1.