MicroRNA-182 prevents vascular smooth muscle cell dedifferentiation via FGF9/PDGFRß signaling.

Authors: Dong, Nana  Wang, Wei  Tian, Jinwei  Xie, Zulong  Lv, Bo  Dai, Jiannan  Jiang, Rui  Huang, Dan  Fang, Shaohong  Tian, Jiangtian  Li, Hulun  Yu, Bo 
Citation: Dong N, etal., Int J Mol Med. 2017 Apr;39(4):791-798. doi: 10.3892/ijmm.2017.2905. Epub 2017 Feb 22.
Pubmed: (View Article at PubMed) PMID:28259995
DOI: Full-text: DOI:10.3892/ijmm.2017.2905

The abnormal phenotypic transformation of vascular smooth muscle cells (SMCs) causes various proliferative vascular diseases. MicroRNAs (miRNAs or miRs) have been established to play important roles in SMC biology and phenotypic modulation. This study revealed that the expression of miR-182 was markedly altered during rat vascular SMC phenotypic transformation in vitro. We aimed to investigate the role of miR-182 in the vascular SMC phenotypic switch and to determine the potential molecular mechanisms involved. The expression of miR-182 gene was significantly downregulated in cultured SMCs during dedifferentiation from a contractile to a synthetic phenotype. Conversely, the upregulation of miR-182 increased the expression of SMC-specific contractile genes, such as α-smooth muscle actin, smooth muscle 22α and calponin. Additionally, miR-182 overexpression potently inhibited SMC proliferation and migration under both basal conditions and under platelet-derived growth factor-BB stimulation. Furthermore, we identified fibroblast growth factor 9 (FGF9) as the target gene of miR-182 for the phenotypic modulation of SMCs mediated through platelet-derived growth factor receptor ß (PDGFRß) signaling. These data suggest that miR-182 may be a novel SMC phenotypic marker and a modulator that may be used to prevent SMC dedifferentiation via FGF9/PDGFRß signaling.

Annotation

Gene Ontology Annotations
Objects Annotated

Additional Information

 
CRRD Object Information
CRRD ID: 13601993
Created: 2018-05-26
Species: All species
Last Modified: 2018-05-26
Status: ACTIVE



NHLBI Logo

RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.