Circ_0008285 silencing suppresses angiotensin II-induced vascular smooth muscle cell apoptosis in thoracic aortic aneurysm via miR-150-5p/BASP1 axis.

Abstract

Vascular smooth muscle cells (VSMCs) are the predominant cell type of the aortic middle layer, the abnormal number or function of which has been demonstrated to have a role in thoracic aortic aneurysm (TAA). Here, this study aimed to identify the function of circ_0008285 in VSMC apoptosis. Human VSMCs were treated with angiotensin II (Ang II) for functional experiments. Cell counting kit-8, 5-ethynyl-2'-deoxyuridine (EdU), and flow cytometry were applied for function analysis. The interaction between miR-150-5p and circ_0008285 or brain acid-soluble protein 1 (BASP1) was also evaluated by dual-luciferase reporter assay and RNA immunoprecipitation assay. Exosomes were isolated by the commercial kit. A highly expressed circ_0008285 was observed in the aortic tissues of TAA patients and Ang-II-induced VSMCs. Circ_0008285 deficiency dramatically reversed Ang-II-induced proliferation arrest and apoptosis promotion in VSMCs. Circ_0008285 functionally targeted miR-150-5p. MiR-150-5p inhibition attenuated the inhibitory effects of circ_0008285 silencing on Ang-II-evoked apoptosis in VSMCs. BASP1 was verified to be a target of miR-150-5p, and was proved to attenuate miR-150-5p-triggered apoptosis arrest in Ang-II-stimulated VSMCs. Additionally, extracellular circ_0008285 was packaged into exosomes, which could be transferred into the recipient cells. Circ_0008285 silencing could suppress Ang-II-induced VSMCs apoptosis via miR-150-5p/BASP1 axis, adding further understanding of the pathogenesis of TAA.