title: Expression changes of activin A in the development of hepatic fibrosis.
abstract: OBJECTIVE
  To examine the expression of activin A, a member of the transforming growth factor (TGFbeta) superfamily, recently has been reported to be overexpressed in liver cirrhosis, in the course of carbon tetrachloride-induced rat hepatic fibrosis.
  
  
  METHODS
  Hepatic fibrosis was induced in rats by subcutaneous injections of 40% carbon tetrachloride oily solution for a period of 1 to 7 weeks. At the end of 1, 2, 3, 4, 5, 6 and 7 weeks after carbon tetrachloride injections, the rats were killed in group (6-10 rats each time) for study. The activin A messenger RNA expression and its protein localization were assessed by semi-quantitative reverse transcription polymerase chain reaction (RT-PCR) and immunohistochemistry.
  
  
  RESULTS
  The normal rat liver expressed activin A mRNA and protein, and its expression was transiently decreased and became undetectable after carbon tetrachloride injections for 2 or 3 weeks and then increased gradually. After injection of carbon tetrachloride for 6 and 7 weeks, activin A mRNA and protein expressions were significantly enhanced in rat liver. Compared with that of the normal rat liver. Activin A mRNA expression levels in rats receiving carbon tetrachloride injections for 6 and 7 weeks were 1.6 and 2.2 times that of those in normal rat liver respectively (0.456 +/- 0.094 vs 0.2860.0670, P< 0.01; 0.620 +/- 0.134 vs 0.286 +/- 0670, P< 0.01). Immunohistochemistry showed that activin A expressed in hepatocytes of normal liver, and its expression was decreased in rats receiving carbon tetrachloride for 2 or 3 weeks. Compared with normal liver, activin A expression distribution mode changed in fibrotic liver, being increased significantly in hepatocytes around fibrotic areas.
  
  
  CONCLUSIONS
  Activin A expression was increased in late stage of hepatic fibrosis, and this may be involved in hepatic fibrosis formation in this period.
authors.affiliation: Gastroenterology Department, Xinhua Hospital, Shanghai Second Medical University, Shanghai 200092, China.
authors.forename: X
authors.initials: X
authors.lastname: Huang
authors.forename: D G
authors.initials: DG
authors.lastname: Li
authors.forename: Z R
authors.initials: ZR
authors.lastname: Wang
authors.forename: H S
authors.initials: HS
authors.lastname: Wei
authors.forename: J L
authors.initials: JL
authors.lastname: Cheng
authors.forename: Y T
authors.initials: YT
authors.lastname: Zhan
authors.forename: X
authors.initials: X
authors.lastname: Zhou
authors.forename: Q F
authors.initials: QF
authors.lastname: Xu
authors.forename: X
authors.initials: X
authors.lastname: Li
authors.forename: H M
authors.initials: HM
authors.lastname: Lu
mesh_terms: D028341:Activins / Q000032:analysis / Q000235:genetics*; D000818:Animals; D002251:Carbon Tetrachloride; D015870:Gene Expression; D007150:Immunohistochemistry; D028322:Inhibin-beta Subunits / Q000032:analysis / Q000235:genetics*; D008099:Liver / Q000737:chemistry / Q000473:pathology; D008103:Liver Cirrhosis / Q000139:chemically induced / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D016133:Polymerase Chain Reaction; D012333:RNA, Messenger / Q000032:analysis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013194:Staining and Labeling
chemical_list: D012333:RNA, Messenger; C422405:activin A; D028341:Activins; D028322:Inhibin-beta Subunits; D002251:Carbon Tetrachloride