期刊
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
卷 400, 期 4, 页码 483-488出版社
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2010.08.067
关键词
miR-155; Adventitial fibroblast; Vascular remodeling
资金
- National Natural Science Foundation of China [30670832, 30870941, 30871085, 8107061]
- National Key Project for Basic Research [2006CB503804, 2009CB521905]
- Shanghai Science and Technology Committee [08JC1417400, 08DZ2200400, 08410702400, 09540704600, 08PJ1408000]
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.
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