Affiliation:
1. Department of Cardiovascular Surgery Heart Center of Henan Provincial People's Hospital, Central China Fuwai Hospital, Central China Fuwai Hospital of Zhengzhou University Zhengzhou China
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.
Subject
Pulmonary and Respiratory Medicine,Oncology,General Medicine
Cited by
2 articles.
订阅此论文施引文献
订阅此论文施引文献,注册后可以免费订阅5篇论文的施引文献,订阅后可以查看论文全部施引文献