Expression of activins, follistatin mRNA in the development of hepatic fibrosis.
- Author:
Xin HUANG
1
;
Dingguo LI
;
Hanming LU
;
Zhirong WANG
;
Hongshan WEI
;
Yuqin WANG
;
Jing ZHANG
;
Qinfang XU
Author Information
- Publication Type:Journal Article
- MeSH: Activins; genetics; Animals; Carbon Tetrachloride; Follistatin; Gene Expression; Inhibin-beta Subunits; genetics; Liver Cirrhosis, Experimental; chemically induced; genetics; pathology; Male; RNA, Messenger; genetics; metabolism; Rats; Rats, Sprague-Dawley; Reverse Transcriptase Polymerase Chain Reaction
- From: Chinese Journal of Hepatology 2002;10(2):85-88
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo examine the expression changes of activin beta A, beta C, beta E and follistatin mRNA in the development of rat hepatic fibrosis induced by carbon tetrachloride (CCl(4)).
METHODSHepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. After carbon tetrachloride injection of 1, 2, 3, 4, 5, 6, and 7 weeks, the 6-12 rats were killed every time. The kinetics of activin beta A, beta C, beta E and follistatin mRNA expression were assessed by the semi-quantity RT-PCR.
RESULTSActivin beta A, beta C, beta E and follistatin mRNA could be detected in normal rat livers. After CCl(4) injection for 2 or 3 weeks, beta A mRNA was transiently decreased and became undetectable, then increased gradually. After CCl injection for 6 and 7 weeks, beta A mRNA level was significantly higher than controls (P<0.01). beta C mRNA could be detected after CCl(4) injection for 1 to 4 weeks and was significantly increased after 5 weeks over controls (P<0.05). beta E mRNA could not be detected after CCl(4) injection for 1 to 5 weeks, but significantly increased after CCl(4) injection for 6 or 7 weeks compared with controls (P<0.01). Except for normal rat liver, no follistatin mRNA was detected in rats after CCl(4) injection.
CONCLUSIONSActivins and follistatin have different expression changes in the development of hepatic fibrosis and the imbalance of activins and follistatin expression may involve in the formation of hepatic fibrosis.