Involvement of miR-145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells

Abstract

Aim: The current study aimed to examine miR-145's contribution to thoracic aortic dissection (AD) development by modulating the biological functions of vascular smooth muscle cells (VSMCs). Methods: The concentration of circulating miR-145 was determined in patients with AD and healthy controls using quantitative polymerase chain reaction (qPCR). Aortic specimens were obtained from both individuals with Stanford type A AD undergoing surgical treatment and deceased organ donors (serving as controls) whose causes of death were nonvascular diseases. Then, qPCR and fluorescence in situ hybridization were applied to assess miR-145 amounts and location, respectively. Furthermore, qPCR and immunoblot were employed to determine SMAD3 (the target gene of miR-145, involved in the TGF-β pathway) amounts at the gene and protein levels, respectively. Moreover, in vitro transfection of VSMCs with miR-145 mimics or inhibitors was conducted. Finally, the 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) assay, Transwell assay and flow cytometry were employed for detecting VSMC proliferation, migration, and apoptosis, respectively. Results: The amounts of miR-145 in plasma and aortic specimens were markedly reduced in the AD group in comparison with control values (P