Open AccessMicro RNA ‐203 negatively regulates c‐Abl, ERK 1/2 phosphorylation, and proliferation in smooth muscle cells
Author(s) -
Liao Guoning,
Panettieri Reynold A.,
Tang Dale D.
Publication year - 2015
Publication title -
physiological reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.918
H-Index - 39
ISSN - 2051-817X
DOI - 10.14814/phy2.12541
Subject(s) - microrna , transfection , cell growth , platelet derived growth factor receptor , phosphorylation , microbiology and biotechnology , messenger rna , vascular smooth muscle , untranslated region , abl , tyrosine phosphorylation , biology , tyrosine kinase , signal transduction , growth factor , cell culture , endocrinology , gene , receptor , smooth muscle , biochemistry , genetics
The nonreceptor tyrosine kinase c‐Abl has a role in regulating smooth muscle cell proliferation, which contributes to the development of airway remodeling in chronic asthma. Micro RNA s (miRs) are small noncoding RNA molecules that regulate gene expression by binding to complementary sequences in the 3′ untranslated regions (3′ UTR ) of target mRNA s. Previous analysis suggests that miR‐203 is able to bind to the 3′ UTR of human c‐Abl mRNA . In this report, treatment with miR‐203 attenuated the expression of c‐Abl mRNA and protein in human airway smooth muscle ( HASM ) cells. Furthermore, transfection with an miR‐203 inhibitor enhanced the expression of c‐Abl at mRNA and protein levels in HASM cells. Treatment with platelet‐derived growth factor ( PDGF ) induced the proliferation and ERK 1/2 phosphorylation in HASM cells. Exposure to miR‐203 attenuated the PDGF ‐stimulated proliferation and ERK 1/2 phosphorylation in HASM cells. The expression of c‐Abl at protein and mRNA levels was higher in asthmatic HASM cells, whereas the level of miR‐203 was reduced in asthmatic HASM cells as compared to control HASM cells. Taken together, our present results suggest that miR‐203 is a negative regulator of c‐Abl expression in smooth muscle cells. miR‐203 regulates smooth muscle cell proliferation by controlling c‐Abl expression, which in turn modulates the activation of ERK1/2.