Downregulation of miR‑142‑5p inhibits human aortic smooth muscle cell proliferation and migration by targeting MKL2

miR-142-5p 下调通过靶向 MKL2 抑制人主动脉平滑肌细胞增殖和迁移

阅读:10
作者:Wei Wu, Yuqiang Shang, Shiling Dai, Chunjun Yu, Jie Wang

Abstract

The increased proliferation and migration of vascular smooth muscle cells (VSMCs) are critical in the progression of atherosclerosis (AS). Platelet‑derived growth factor type BB (PDGF‑BB) may induce VSMC proliferation and migration. miR‑142‑5p plays a critical role in various biological processes, including tumorigenesis, angiogenesis and inflammation. However, whether miR‑142‑5p is involved in regulating the pathological process of arteriosclerosis remains to be elucidated. Therefore, in this study, the role of miR‑142‑5p in PDGF‑BB‑induced human aortic smooth muscle cell (HSAMC) proliferation and migration was investigated. The results revealed that the expression level of miR‑142‑5p was enhanced in the serum of patients with AS, while that of its target gene, myocardin‑like protein 2 (MKL2) was decreased, compared with that in healthy volunteers. Moreover, there was a negative correlation between miR‑142‑5p and MKL2 expression in the serum of patients with AS. Furthermore, the downregulation of miR‑142‑5p inhibited PDGF‑BB‑induced HASMC proliferation and migration; however, the inhibition of HASMC proliferation and migration was reversed by co‑transfection with small interfering RNA (siRNA) against MKL2 (siRNA‑MKL2). In addition, transfection with miR‑142‑5p inhibitor significantly increased the expression levels of MKL2, and decreased those of matrix metalloproteinase (MMP)2 and 9, and these effects were reversed by transfection with siRNA‑MKL2. Finally, MKL2 was proven to be a target of miR‑142‑5p. On the whole, the findings of the present study demonstrate that the downregulation of miR‑142‑5p inhibits human aortic smooth muscle cell (HSAMC) proliferation and migration possibly by targeting MKL2. Hence, miR‑142‑5p may prove to be a novel therapeutic target in the treatment of AS.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。