MicroRNA-155 regulates angiotensin II type 1 receptor expression and phenotypic differentiation in vascular adventitial fibroblasts
| Autor: | Weili Shen, Li-Min Zhu, Wen-Dong Chen, Liang Zheng, Dingliang Zhu, Cheng-Chao Ruan, Pingjin Gao, Chan-Chan Xu |
|---|---|
| Rok vydání: | 2010 |
| Předmět: |
medicine.medical_treatment
Receptor expression Biophysics Down-Regulation Aorta Thoracic Biology Biochemistry Receptor Angiotensin Type 1 Rats Sprague-Dawley miR-155 Downregulation and upregulation microRNA medicine Animals Phosphorylation Luciferases Molecular Biology Cells Cultured Mitogen-Activated Protein Kinase 1 Regulation of gene expression Mitogen-Activated Protein Kinase 3 Angiotensin II Growth factor Cell Differentiation Cell Biology Fibroblasts Molecular biology Rats MicroRNAs Gene Expression Regulation Hypertension Myofibroblast |
| Zdroj: | Biochemical and Biophysical Research Communications. 400:483-488 |
| ISSN: | 0006-291X |
| DOI: | 10.1016/j.bbrc.2010.08.067 |
| Popis: | 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 (AT1R) is a miR-155 target gene. The present study investigated the potential role of miR-155 in regulating AT1R expression and phenotypic differentiation in rat aortic adventitial fibroblasts (AFs). Luciferase assay demonstrated that miR-155 suppressed AT1R 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 AT1R expression. |
| Databáze: | OpenAIRE |
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