Document Detail


MicroRNA-155 regulates angiotensin II type 1 receptor expression and phenotypic differentiation in vascular adventitial fibroblasts.
MedLine Citation:
PMID:  20735984     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
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 α-smooth muscle actin (α-SMA, produces myofibroblast) expression, but did not transform growth factor beta-1 (TGF-β1). 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.
Authors:
Liang Zheng; Chan-Chan Xu; Wen-Dong Chen; Wei-Li Shen; Cheng-Chao Ruan; Li-Min Zhu; Ding-Liang Zhu; Ping-Jin Gao
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-22
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  400     ISSN:  1090-2104     ISO Abbreviation:  Biochem. Biophys. Res. Commun.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-10-04     Completed Date:  2010-11-23     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  United States    
Other Details:
Languages:  eng     Pagination:  483-8     Citation Subset:  IM    
Copyright Information:
Copyright © 2010 Elsevier Inc. All rights reserved.
Affiliation:
State Key Laboratory of Medical Genomics, Shanghai Key Laboratory of Vascular Biology and Department of Hypertension, Ruijin Hospital, Shanghai Jiao Tong University School of Medicine, China.
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MeSH Terms
Descriptor/Qualifier:
Angiotensin II / metabolism,  pharmacology
Animals
Aorta, Thoracic / cytology*,  metabolism
Cell Differentiation / genetics*
Cells, Cultured
Down-Regulation
Fibroblasts / cytology*,  metabolism
Gene Expression Regulation*
Hypertension / genetics*
Luciferases / genetics
MicroRNAs / genetics,  metabolism*
Mitogen-Activated Protein Kinase 1 / metabolism
Mitogen-Activated Protein Kinase 3 / metabolism
Phosphorylation
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 / genetics*
Chemical
Reg. No./Substance:
0/MicroRNAs; 0/Receptor, Angiotensin, Type 1; 11128-99-7/Angiotensin II; EC 1.13.12.-/Luciferases; EC 2.7.11.24/Mitogen-Activated Protein Kinase 1; EC 2.7.11.24/Mitogen-Activated Protein Kinase 3

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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