Open AccessInvolvement of miR‐145 in the development of aortic dissection via inducing proliferation, migration, and apoptosis of vascular smooth muscle cells
Author(s) -
Huang Wenhui,
Huang Cheng,
Ding Huanyu,
Luo Jianfang,
Liu Yuan,
Fan Ruixin,
Xiao Fei,
Fan Xiaoping,
Jiang Zhisheng
Publication year - 2020
Publication title -
journal of clinical laboratory analysis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.536
H-Index - 50
eISSN - 1098-2825
pISSN - 0887-8013
DOI - 10.1002/jcla.23028
Subject(s) - apoptosis , vascular smooth muscle , downregulation and upregulation , flow cytometry , transfection , cell growth , real time polymerase chain reaction , in vitro , microrna , biology , microbiology and biotechnology , chemistry , cancer research , gene , endocrinology , smooth muscle , biochemistry
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 < .05). miR‐145 was mostly located in VSMCs. Proliferation and apoptosis of VSMCs were significantly induced in vitro by the downregulation of miR‐145. Also, miR‐145 modulated SMAD3 expression. Conclusions miR‐145 was found to be downregulated in patients with AD, which induced the proliferation, migration, and apoptosis of VSMCs by targeting SMAD3. This suggested the involvement of miR‐145 in the pathogenesis of AD.