PMID- 18158920
OWN - NLM
STAT- MEDLINE
DCOM- 20080307
LR  - 20161124
IS  - 1090-2104 (Electronic)
IS  - 0006-291X (Linking)
VI  - 367
IP  - 1
DP  - 2008 Feb 29
TI  - Canonical Wnt signaling maintains the quiescent stage of hepatic stellate cells.
PG  - 116-23
AB  - It is well known that hepatic stellate cells (HSC) develop into cells, which are 
      thought to contribute to liver fibrogenesis. Recent data suggest that HSC are 
      progenitor cells with the capacity to differentiate into cells of endothelial and 
      hepatocyte lineages. The present study shows that beta-catenin-dependent 
      canonical Wnt signaling is active in freshly isolated HSC of rats. Mimicking of 
      the canonical Wnt pathway in cultured HSC by TWS119, an inhibitor of the glycogen 
      synthase kinase 3beta, led to reduced beta-catenin phosphorylation, induced 
      nuclear translocation of beta-catenin, elevated glutamine synthetase production, 
      impeded synthesis of alpha-smooth muscle actin and Wnt5a, but promoted the 
      expression of glial fibrillary acidic protein, Wnt10b, and paired-like 
      homeodomain transcription factor 2c. In addition, canonical Wnt signaling lowered 
      DNA synthesis and hindered HSC from entering the cell cycle. The findings 
      demonstrate that beta-catenin-dependent Wnt signaling maintains the quiescent 
      state of HSC and, similar to stem and progenitor cells, influences their 
      developmental fate.
FAU - Kordes, Claus
AU  - Kordes C
AD  - Clinic of Gastroenterology, Hepatology and Infectiology, 
      Heinrich-Heine-University, Moorenstrasse 5, 40225 Dusseldorf, Germany.
FAU - Sawitza, Iris
AU  - Sawitza I
FAU - Haussinger, Dieter
AU  - Haussinger D
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20071226
PL  - United States
TA  - Biochem Biophys Res Commun
JT  - Biochemical and biophysical research communications
JID - 0372516
RN  - 0 (Actins)
RN  - 0 (Enzyme Inhibitors)
RN  - 0 (Glial Fibrillary Acidic Protein)
RN  - 0 (Paired Box Transcription Factors)
RN  - 0 (Wnt Proteins)
RN  - 0 (beta Catenin)
RN  - EC 2.7.11.1 (Glycogen Synthase Kinase 3 beta)
RN  - EC 2.7.11.1 (Gsk3b protein, rat)
RN  - EC 2.7.11.26 (Glycogen Synthase Kinase 3)
RN  - EC 6.3.1.2 (Glutamate-Ammonia Ligase)
SB  - IM
MH  - Actins/metabolism
MH  - Animals
MH  - Enzyme Inhibitors/pharmacology
MH  - Gene Expression Regulation/genetics/physiology
MH  - Glial Fibrillary Acidic Protein/genetics/metabolism
MH  - Glutamate-Ammonia Ligase/metabolism
MH  - Glycogen Synthase Kinase 3/antagonists & inhibitors
MH  - Glycogen Synthase Kinase 3 beta
MH  - Hepatocytes/cytology/*metabolism/pathology
MH  - Immunohistochemistry
MH  - Liver Cirrhosis/*metabolism/pathology
MH  - Male
MH  - Paired Box Transcription Factors/genetics/metabolism
MH  - Phosphorylation
MH  - Rats
MH  - Rats, Wistar
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction/genetics/*physiology
MH  - Stem Cells/metabolism
MH  - Wnt Proteins/genetics/*metabolism
MH  - beta Catenin/genetics/*metabolism
EDAT- 2007/12/27 09:00
MHDA- 2008/03/08 09:00
CRDT- 2007/12/27 09:00
PHST- 2007/12/10 00:00 [received]
PHST- 2007/12/14 00:00 [accepted]
PHST- 2007/12/27 09:00 [pubmed]
PHST- 2008/03/08 09:00 [medline]
PHST- 2007/12/27 09:00 [entrez]
AID - S0006-291X(07)02746-5 [pii]
AID - 10.1016/j.bbrc.2007.12.085 [doi]
PST - ppublish
SO  - Biochem Biophys Res Commun. 2008 Feb 29;367(1):116-23. doi: 
      10.1016/j.bbrc.2007.12.085. Epub 2007 Dec 26.