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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 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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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. |
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ISSN: | 0006-291X 1090-2104 |
DOI: | 10.1016/j.bbrc.2010.08.067 |