Linping Zhang1, Gang Jin1, Wei Zhang1, Xiaoming Wang1, Zhenjiang Li1, Qianlan Dong2. 1. Kidney Disease and Dialysis Center, Shaanxi Provincial People's Hospital, No. 256 Youyi West Road, Beilin District, Xi'an, 710068, Shaanxi, China. 2. Kidney Disease and Dialysis Center, Shaanxi Provincial People's Hospital, No. 256 Youyi West Road, Beilin District, Xi'an, 710068, Shaanxi, China. dcak8nf@163.com.
Abstract
BACKGROUND: Hsa_circ_0080425 (circ_0080425) is newly identified to correlate with the progression of diabetic nephropathy (DN). However, its role and mechanism in DN process is not very clear. METHODS: Cell counting kit-8 assay, flow cytometry, scratch wound assay, and western blotting were performed to measure endothelial cell dysfunction. Expression of circ_0080425, microRNA (miR)-140-3p and fibronectin 1 (FN1) were determined by quantitative real-time PCR and western blotting. The direct interaction was confirmed by dual-luciferase reporter assay. RESULTS: High-glucose (HG) treatment could induce inhibition of cell proliferation, cell cycle entrance and wound healing rate in human umbilical vein endothelial cells (HRGEC), and enhancement of apoptosis rate. Circ_0080425 expression was upregulated by HG, and exhausting circ_0080425 could attenuate HG-induced above effects in HRGEC. MiR-140-3p was sponged by circ_0080425, and its inhibitor reversed the regulation of circ_0080425 knockdown on HG-induced HRGEC injury. FN1 was targeted by miR-140-3p, and its overexpression also restored the inhibitory effect of miR-140-3p on HC-induced HRGEC injury. CONCLUSION: Circ_0080425 expression might contribute to HG-induced endothelial cell injury, and circ_0080425/miR-140-3p/FN1 axis was a potential therapeutic approach to interfere DN process.
BACKGROUND: Hsa_circ_0080425 (circ_0080425) is newly identified to correlate with the progression of diabetic nephropathy (DN). However, its role and mechanism in DN process is not very clear. METHODS: Cell counting kit-8 assay, flow cytometry, scratch wound assay, and western blotting were performed to measure endothelial cell dysfunction. Expression of circ_0080425, microRNA (miR)-140-3p and fibronectin 1 (FN1) were determined by quantitative real-time PCR and western blotting. The direct interaction was confirmed by dual-luciferase reporter assay. RESULTS: High-glucose (HG) treatment could induce inhibition of cell proliferation, cell cycle entrance and wound healing rate in human umbilical vein endothelial cells (HRGEC), and enhancement of apoptosis rate. Circ_0080425 expression was upregulated by HG, and exhausting circ_0080425 could attenuate HG-induced above effects in HRGEC. MiR-140-3p was sponged by circ_0080425, and its inhibitor reversed the regulation of circ_0080425 knockdown on HG-induced HRGEC injury. FN1 was targeted by miR-140-3p, and its overexpression also restored the inhibitory effect of miR-140-3p on HC-induced HRGEC injury. CONCLUSION: Circ_0080425 expression might contribute to HG-induced endothelial cell injury, and circ_0080425/miR-140-3p/FN1 axis was a potential therapeutic approach to interfere DN process.