文献类型：期刊文献

英文题名：MicroRNA-145 Mediates the Formation of Angiotensin II-Induced Murine Abdominal Aortic Aneurysm

作者：Wu, Jing[1];Wang, Jun[3];Li, Xiaoou[4];Liu, Xiaofeng[4];Yu, Xiuyan[4];Tian, Yunling[2]

第一作者：吴晶

通信作者：Tian, YL[1]

机构：[1]Gansu Univ Chinese Med, Sch Nursing, Lanzhou 730000, Peoples R China;[2]Lanzhou Univ, Hosp 1, Lanzhou 730000, Peoples R China;[3]Shenzhen Ctr Chron Dis Control, Shenzhen 518020, Peoples R China;[4]Tumor Hosp Jilin Prov, Changchun 130021, Peoples R China

第一机构：甘肃中医药大学护理学院

通信机构：[1]corresponding author), Lanzhou Univ, Hosp 1, Dept Endocrinol, 1 Dong Gang West Rd, Lanzhou 730000, Peoples R China.

年份：2017

卷号：26

期号：6

起止页码：619

外文期刊名：HEART LUNG AND CIRCULATION

收录：;Scopus(收录号：2-s2.0-85008224779);WOS:【SCI-EXPANDED(收录号:WOS:000402467300014)】；

基金：This work was supported by Natural Science Foundation of Gansu Province, China (2014GS030970), Health and Family Planning Commission of Gansu Province (GSWSKY2016-31), Health and Family Planning Commission of Jilin Province (2013ZC042), and the National High Technology Research and Development Program ("863" Program) of China (2011AA02A111).

语种：英文

外文关键词：MicroRNA-145; Aneurysm; MMP2

摘要：Background MicroRNA-145 (miR-145) has been implicated in vascular smooth muscle cell differentiation, but the underlying mechanisms have not been fully understood, especially their role in abdominal aortic aneurysm (AAA) expansion. Here, we sought to explore and define the mechanisms of miR-145 function in the experimental AAA models in AngII-infused ApoE(-/-) mice. Methods miR-145 was overexpressed in ApoE(-/-) mice via lentivirus infection, and then the incidence of AAA, maximum abdominal aortic diameter, elastin degradation and MMP2 activation were determined in AngII-infused ApoE(-/-) mice. Results In vivo overexpression of miR-145 by lentivirus infection greatly decreased the incidence of AAA, maximum abdominal aortic diameter, and elastin degradation, accompanied with downregulation of MMP2 activation in AngII-infused ApoE(-/-) mice. Cell culture assays indicated that miR-145 inhibited AngII-induced upregulation of MMP2 gene expression. In contrast, deficiency of MMP2 abolished the effects of miR-145 on AngII-induced elastin and collagens degradations in ApoE(-/-) mice. Conclusion These data suggest that regulation of expression of miR-145 may be a potential therapeutic option for vascular disease progression such as AAA expansion.