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

► We reported that miR-155 can markedly decrease the expression of AT 1R protein in vascular AFs. ► Our experiments suggest miR-155 may play a role in Ang II induced phenotypic differentiation via AT 1R. ► According to our results, miR-155 might spark off great interest in diagnosis and therapy of c...

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Published in:Biochemical and biophysical research communications 2010-10, Vol.400 (4), p.483-488
Main Authors: Zheng, Liang, Xu, Chan-Chan, Chen, Wen-Dong, Shen, Wei-Li, Ruan, Cheng-Chao, Zhu, Li-Min, Zhu, Ding-Liang, Gao, Ping-Jin
Format: Article
Language:English
Subjects:
Actin
Adventitial fibroblast
Angiotensin II - metabolism
Angiotensin II - pharmacology
Animals
Aorta, Thoracic - cytology
Aorta, Thoracic - metabolism
Cell Differentiation - genetics
Cells, Cultured
Down-Regulation
Fibroblasts - cytology
Fibroblasts - metabolism
Gene Expression Regulation
Hypertension - genetics
Luciferases - genetics
MicroRNAs - genetics
MicroRNAs - metabolism
miR-155
Mitogen-Activated Protein Kinase 1 - metabolism
Mitogen-Activated Protein Kinase 3 - metabolism
Phosphorylation
Rats
Rats, Sprague-Dawley
Receptor, Angiotensin, Type 1 - genetics
Vascular remodeling
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Summary:► We reported that miR-155 can markedly decrease the expression of AT 1R protein in vascular AFs. ► Our experiments suggest miR-155 may play a role in Ang II induced phenotypic differentiation via AT 1R. ► According to our results, miR-155 might spark off great interest in diagnosis and therapy of cardiovascular diseases. 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 1R) is a miR-155 target gene. The present study investigated the potential role of miR-155 in regulating AT 1R expression and phenotypic differentiation in rat aortic adventitial fibroblasts (AFs). Luciferase assay demonstrated that miR-155 suppressed AT 1R 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 1R expression.
ISSN:0006-291X
1090-2104
DOI:10.1016/j.bbrc.2010.08.067