Circ_0000345 Protects Endothelial Cells From Oxidized Low-Density Lipoprotein-Induced Injury by miR-129-5p/Ten-Eleven Translocation Axis.

Circular RNAs have shown regulatory functions in atherosclerosis (AS) progression. Here, we explored the role and working mechanism of circ_0000345 in the AS cell model in vitro. Quantitative real-time polymerase chain reaction was applied to measure the enrichment of circ_0000345, microRNA-129-5p (miR-129-5p), and ten-eleven translocation-2 (TET2) messenger RNA. Cell Counting Kit 8 assay was used to analyze cell viability of human umbilical vein endothelial cells (HUVECs). Flow cytometry was conducted to assess cell apoptosis and cell cycle progression. The target relationship between miR-129-5p and circ_0000345 or TET2 was verified by the dual-luciferase reporter assay. The Western blot assay was used to analyze the protein level of TET2. Circ_0000345 abundance was reduced in serum samples of AS patients and AS cell model compared with their matching counterparts. Circ_0000345 overexpression promoted cell viability and cell cycle progression and hampered cell apoptosis in HUVECs induced by oxidized low-density lipoprotein. MiR-129-5p was a target of circ_0000345 and circ_0000345 attenuated ox-LDL-induced damage in HUVECs through sponging miR-129-5p. MiR-129-5p bound to the 3' untranslated region (3'UTR) of TET2, and miR-129-5p functioned in ox-LDL-induced HUVECs by targeting TET2. Circ_0000345 enhanced TET2 messenger RNA and protein expression through sponging miR-129-5p in HUVECs. Circ_0000345 attenuated ox-LDL-mediated injury in HUVECs through targeting miR-129-5p/TET2 axis. Increasing the levels of circ_0000345 and TET2 might be a novel insight into AS treatment.