Knockdown of circ_0004104 Alleviates Oxidized Low-Density Lipoprotein-Induced Vascular Endothelial Cell Injury by Regulating miR-100/TNFAIP8 Axis

Abstract: Coronary artery disease (CAD) is a common cardiovascular disease, mainly due to vascular endothelial cell (VEC) injury caused by atherosclerosis. Circular RNA has been shown to be involved in the regulation of various diseases. However, the role and mechanism of circ_0004104 in CAD are still unclear. Oxidized low-density lipoprotein (ox-LDL) was used to construct the VEC injury model in vitro. The expression levels of circ_0004104 and miR-100 were measured by quantitative real-time polymerase chain reaction. The proliferation of VECs was determined using 3-(45)-dimethylthiahiazo (-z-y1)-35-di-phenytetrazoliumromide assay and 5-ethynyl-2′-deoxyuridine staining assay. VEC apoptosis rate was assessed using flow cytometry, and caspase-3 activity was measured using a Caspase-3 Assay Kit. The protein expression levels of Ki-67, cleaved-caspase3, and tumor necrosis factor-α-induced protein 8 (TNFAIP8) were detected by western blot analysis. Furthermore, enzyme-linked immunosorbent assay was performed to assess the concentrations of inflammatory cytokines. In addition, the relationship between miR-100 and circ_0004104 or TNFAIP8 was confirmed by dual-luciferase reporter assay and biotin-labeled RNA pull-down assay. Our results revealed that circ_0004104 was upregulated and miR-100 was downregulated in patients with CAD and ox-LDL–induced VECs. Ox-LDL could inhibit the proliferation and promote the apoptosis and inflammation of VECs to induce VEC injury. However, si...
Source: Journal of Cardiovascular Pharmacology - Category: Cardiology Tags: Original Article Source Type: research