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

Abstract

AbstractBackgroundVascular 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.MethodsHuman 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.ResultsA 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.ConclusionCirc_0008285 silencing could suppress Ang‐II‐induced VSMCs apoptosis via miR‐150‐5p/BASP1 axis, adding further understanding of the pathogenesis of TAA.