Circ_0091822 aggravates ox-LDL-induced endothelial cell injury through targeting the miR-661/RAB22A axis

BACKGROUND: Endothelial dysfunction is considered to be an important factor in the pathogenesis of atherosclerosis. Circular RNAs (circRNAs) have been confirmed to participate in the development of atherosclerosis. Nevertheless, the role and mechanism of circ 0091822 in atherosclerosis have not been studied yet. METHODS: The expression of circ 0091822, miR-661 and RAB22A were analyzed by quantitative real-time polymerase chain reaction (qRT-PCR). The levels of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were estimated by enzymelinked immunosorbent assay (ELISA). Cell viability was analyzed by Cell Counting Kit-8 (CCK-8) assay, cell proliferation was evaluated by EdU assay, and cell apoptosis was gauged by flow cytometry. Western blot was performed to assess the protein levels of Bax, Cleaved-caspase-3 and RAB22A. The interaction among miR-661 and circ 0091822 or RAB22A was verified by dual-luciferase reporter assay RESULTS: Ox-LDL enhanced the expression of circ 0091822 in HUVECs. It also constrained proliferation, promotes apoptosis and inflammation in HUVECs, and down-regulation of circ 0091822 attenuated these effects. Mechanically, circ 0091822 could serve as a sponge of miR-661, miR-661 interference rescued circ 0091822 inhibition-mediated effect on the biological functions in ox-LDL-induced HUVECs. Additionally, RAB22Awas a target of miR-661, and its overexpression could partially overturn the negative regulation of miR-661 on ox-LDL-treated HUVECs injury. Importantly, circ 0091822 sponged miR-661 to positively regulate RAB22A expression. CONCLUSION: Circ 0091822 contributed to cell injury by targeting miR-661/RAB22A axis in ox-LDL-stimulated HUVECs.