MicroRNA-155 regulates angiotensin II type 1 receptor expression and phenotypic differentiation in vascular adventitial fibroblasts

被引：151

作者：

Zheng, Liang ^{[1
,2
]}

Xu, Chan-Chan ^{[1
,2
,5
]}

Chen, Wen-Dong ^{[1
,2
]}

Shen, Wei-Li ^{[1
,2
,3
]}

Ruan, Cheng-Chao ^{[3
]}

Zhu, Li-Min ^{[1
,2
,4
]}

Zhu, Ding-Liang ^{[1
,2
,3
,4
]}

Gao, Ping-Jin ^{[1
,2
,3
,4
]}

机构：

[1] Shanghai Jiao Tong Univ, Ruijin Hosp, Shanghai Key Lab Vasc Biol, State Key Lab Med Genom,Sch Med, Shanghai 200025, Peoples R China

[2] Shanghai Jiao Tong Univ, Ruijin Hosp, Dept Hypertens, Sch Med, Shanghai 200025, Peoples R China

[3] Chinese Acad Sci, Shanghai Inst Biol Sci, Inst Hlth Sci, Lab Vasc Biol, Shanghai, Peoples R China

[4] Shanghai Res Inst Hypertens, Shanghai, Peoples R China

[5] Shanghai Jiao Tong Univ, Shanghai Hosp 6, Dept Geriatr, Shanghai 200030, Peoples R China

来源：

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS | 2010年 / 400卷 / 04期

基金：

中国国家自然科学基金;

关键词：

miR-155; Adventitial fibroblast; Vascular remodeling; MYOFIBROBLASTS; INVOLVEMENT;

D O I：

10.1016/j.bbrc.2010.08.067

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

070307 [化学生物学]; 071010 [生物化学与分子生物学];

摘要：

MicroRNAs (miRNAs), which are genomically encoded small RNAs, negatively regulate target gene expression at the post-transcriptional level. Our recent study indicated that microRNA-155 (miR-155) might be negatively correlated with blood pressure, and it has been suggested that miR-155-mediated target genes could be involved in the cardiovascular diseases. Bioinformatic analyses predict that angiotensin II type 1 receptor (AT(1)R) is a miR-155 target gene. The present study investigated the potential role of miR-155 in regulating AT(1)R expression and phenotypic differentiation in rat aortic adventitial fibroblasts (AFs). Luciferase assay demonstrated that miR-155 suppressed AT(1)R 3'-UTR reporter construct activity. miR-155 overexpression in AFs did not reduce target mRNA levels, but significantly reduced target protein expression. In addition, AFs transfected with pSUPER/miR-155 exhibited reduced Ang II-induced ERK1/2 activation. miR-155 overexpression in cells attenuated Ang II-induced alpha-smooth muscle actin (alpha-SMA, produces myofibroblast) expression, but did not transform growth factor beta-1 (TGF-beta 1). This study demonstrated that miR-155 could have an important role in regulating adventitial fibroblast differentiation and contribute to suppression of AT(1)R expression. (C) 2010 Elsevier Inc. All rights reserved.

引用

页码：483 / 488

页数：6

共 22 条

[1]

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