Smad7 inhibits collagen expression in human hepatic satellite cells in vitro.
- Author:
Li-xia TANG
1
;
Guang YANG
;
Jia-ju TANG
Author Information
- Publication Type:Journal Article
- MeSH: Actins; genetics; metabolism; Cells, Cultured; Collagen Type I; genetics; metabolism; Genetic Therapy; Hepatocytes; cytology; metabolism; Humans; Liver Cirrhosis; metabolism; therapy; Smad7 Protein; pharmacology; Transforming Growth Factor beta1; pharmacology
- From: Journal of Southern Medical University 2009;29(10):2122-2127
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the effect of Smad7 on the expressions of collagen I and alpha-smooth muscle actin (alpha-SMA) in HSC-T6 cell line activated by transforming growth factor-beta1 (TGF-beta1).
METHODSHSC-T6 cells stably expressing M2-flag protein were selected after co-infection of the cells with pTRE-Smad7-M2-flag and pTet-on. The optimal dose of doxycycline for inducing Smad7 was determined, and the effects of Smad7 over-expression on the expressions of collagen I and alpha-SMA in the cells activated by TGF-beta1 and on Smad2/3 phosphorylation were evaluated using Western blotting.
RESULTSThe optimal dose of doxycycline for inducing Smad7 expression was 2 mg/L. Smad7 over-expression induced by doxycycline decreased the expressions of collagen I and alpha-SMA in HSC-T6 cells activated by TGF-beta1, and down-regulated the level of Smad2/3 phosphorylation.
CONCLUSIONSmad7 over-expression inhibits Smad2/3 phosphorylation, and decreases the expression of collagen I and alpha-SMA in HSC-T6 cells induced by TGF-beta1 to inhibit the progression of liver fibrosis.
