PMID- 7875675
OWN - NLM
STAT- MEDLINE
DCOM- 19950404
LR  - 20061115
IS  - 0270-9139 (Print)
IS  - 0270-9139 (Linking)
VI  - 21
IP  - 3
DP  - 1995 Mar
TI  - Transforming growth factor-beta 1 (TGF-beta 1) and TGF-beta 1 receptors in 
      normal, cirrhotic, and neoplastic human livers.
PG  - 760-6
AB  - Transforming growth factor-Beta 1 (TGF-beta 1) is an important mediator of 
      control of liver cell proliferation and replication. The aim of the current study 
      was to compare TGF-beta 1 gene expression, protein synthesis, and cell membrane 
      receptors in normal liver, cirrhotic nodules, and neoplastic human livers. Five 
      surgical resections for metastasis in an otherwise normal liver and 25 resections 
      for hepatocellular carcinoma with cirrhosis were included in this study. 
      Messenger RNA (mRNA) and TGF-beta 1 protein were detected on serial tissue 
      sections of normal, cirrhotic, and tumoral livers using in situ hybridization and 
      immunohistochemistry. TGF-beta 1 type II receptors were detected on tissue 
      sections using immunohistochemistry. In normal livers, TGF-beta 1 mRNA and 
      protein were not significantly expressed. In cirrhotic nodules, a few sinusoidal 
      cells and mesenchymal cells of fibrous septa displayed TGF-beta 1 mRNA. By 
      immunohistochemistry, protein was detected in the extracellular matrix along the 
      fibrous septa. Hepatocytes from normal and cirrhotic livers did not express 
      TGF-beta 1. In contrast, the cytoplasm of hepatocytes in neoplastic nodules 
      showed intense staining for TGF-beta 1 mRNA and protein. Although TGF-beta 1 
      receptor II was expressed on the plasma membrane of normal liver cells, tumoral 
      hepatocytes no longer displayed membrane labeling but rather diffuse 
      intracytoplasmic staining with perinuclear accumulation. This study suggests that 
      the escape of tumoral hepatocytes from control of cell proliferation by TGF-beta 
      1, despite its overexpression by these cells, might be related to a defect in 
      TGF-beta 1 receptor II processing on the liver cell membrane.
FAU - Bedossa, P
AU  - Bedossa P
AD  - Laboratoire d'Anatomie Pathologique, Hopital de Bicetre, Paris, France.
FAU - Peltier, E
AU  - Peltier E
FAU - Terris, B
AU  - Terris B
FAU - Franco, D
AU  - Franco D
FAU - Poynard, T
AU  - Poynard T
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United States
TA  - Hepatology
JT  - Hepatology (Baltimore, Md.)
JID - 8302946
RN  - 0 (Receptors, Transforming Growth Factor beta)
RN  - 0 (Transforming Growth Factor beta)
SB  - IM
MH  - Carcinoma, Hepatocellular/metabolism/pathology
MH  - Female
MH  - Humans
MH  - Immunohistochemistry
MH  - In Situ Hybridization
MH  - Liver/cytology/*metabolism/pathology
MH  - Liver Cirrhosis/*metabolism/pathology
MH  - Liver Neoplasms/*metabolism/pathology
MH  - Male
MH  - Middle Aged
MH  - Receptors, Transforming Growth Factor beta/*metabolism
MH  - Reference Values
MH  - Transforming Growth Factor beta/*metabolism
EDAT- 1995/03/01 00:00
MHDA- 1995/03/01 00:01
CRDT- 1995/03/01 00:00
PHST- 1995/03/01 00:00 [pubmed]
PHST- 1995/03/01 00:01 [medline]
PHST- 1995/03/01 00:00 [entrez]
AID - 0270-9139(95)90530-8 [pii]
PST - ppublish
SO  - Hepatology. 1995 Mar;21(3):760-6.