miR-92a regulates the expression levels of matrix metalloproteinase 9 and tissue inhibitor of metalloproteinase 3 via sirtuin 1 signaling in hydrogen peroxide-induced vascular smooth muscle cells

miR-92a 通过 sirtuin 1 信号调节过氧化氢诱导的血管平滑肌细胞中基质金属蛋白酶 9 和组织金属蛋白酶抑制剂 3 的表达水平

阅读:5
作者:Peng Liu, Jianfang Su, Xixi Song, Shixiao Wang

Abstract

Vascular smooth muscle cells (VSMCs) exhibit a notably increased rate of migration, which is one of the most common pathological changes in atherosclerosis. Investigations into the role of micro (mi)RNAs in the regulation of VSMC migration are beginning to emerge and additional miRNAs involved in VSMC migration modulation require identification. In the current study, VSMCs were primarily cultured from rat thoracic aortas, transfected with miR‑92a mimics and induced by hydrogen peroxide (H2O2) for 24 h. Total mRNA and protein were collected for quantitative polymerase chain reaction and western blot analysis. In addition, the sirtuin 1 (SIRT1) gene was detected by luciferase reporter assay and VSMC migration was detected by Transwell migration assay. The current results demonstrated that reduced expression of miR‑92a and overexpression of SIRT1 at the mRNA level were observed in H2O2‑induced VSMCs. Furthermore, luciferase reporter assay demonstrated that the activity of the SIRT1 3'‑untranslated region was reduced by miR‑92a mimics. The upregulation of MMP9 and the downregulation of TIMP3 in H2O2‑induced VSMCs were observed to be reversed by miR‑92a mimics in addition to SIRT1 siRNA. Finally, Transwell migration assay revealed that miR‑92a overexpression and silencing SIRT1 mitigated VSMC migration following H2O2 treatment. The present study indicated that miR‑92a prevented the migration of H2O2‑induced VSMCs by repressing the expression of SIRT1, and also provided a novel therapy to protect against the phenotypic change of VSMCs in atherosclerosis.

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。