Abstract
BackgroundDiabetic 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.MethodsThe 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.ResultscircZNF532 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.ConclusioncircZNF532 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.
Highlights
Diabetic retinopathy (DR) is a common microvascular complication of diabetes leading to impaired vision and blindness, and one-third of diabetic patients suffer from DR [1]
We explored the biological function and potential mechanism of circZNF532 in high glucose-disposed human retinal microvascular endothelial cells (hRMECs), suggesting that the circZNF532/miR-1243/coactivator associated arginine methyltransferase 1 (CARM1) axis might provide new biomarkers for DR treatment
CircZNF532 was overexpressed in high glucose (HG)‐treated hRMECs Subsequently, the effect of glucose on circZNF532 expression in vitro was investigated
Summary
Diabetic retinopathy (DR) is a common microvascular complication of diabetes leading to impaired vision and blindness, and one-third of diabetic patients suffer from DR [1]. Mounting reports have validated that circRNAs exert their functional effects in different diseases via functioning as microRNA (miRNA) sponges [14]. Several reports have corroborated that circRNAs are identified as regulators of DR progression [16]. A previous study found that circRNA zinc finger protein 532 (circZNF532; hsa_circ_0047814) was strikingly upregulated in DR through circular RNA microarrays [19]. Bioinformatics prediction showed that circZNF532 may interact with miR-1243, which is prominently decreased in DR patients [20]. The relationship between circZNF532 and miR-1243 in DR progression remains indistinct. 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
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