Journal
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS
Volume 367, Issue 1, Pages 116-123Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.bbrc.2007.12.085
Keywords
HSC; Ki-67; Lef1; Pitx2; Tef1; TWS119; Wnt
Categories
Ask authors/readers for more resources
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 3 beta, 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, Writ I Ob, and paired-like homeodomain transcription factor 2c. In addition, canonical Writ signaling lowered DNA synthesis and hindered HSC from entering the cell cycle. The findings demonstrate that beta-catenin-dependent Writ signaling maintains the quiescent state of HSC and, similar to stem and progenitor cells, influences their developmental fate. (C) 2007 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available