ArticleThe American journal of pathology2008
Divergent transforming growth factor-beta signaling in hepatic stellate cells after liver injury: functional effects on ECE-1 regulation.
Article in The American journal of pathology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers, 1 of them a synthesis that pooled it.
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Who cites it
14 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Deciphering Molecular Mechanisms of Carbon Tetrachloride- Induced Hepatotoxicity: A Brief Systematic Review.Current molecular medicine · 2024Pooled it
- Unraveling the hepatic stellate cells mediated mechanisms in aging's influence on liver fibrosis.Scientific reports · 2024Article
- Induction of E6AP by microRNA-302c dysregulation inhibits TGF-β-dependent fibrogenesis in hepatic stellate cells.Scientific reports · 2020Article
- Hepatic stellate cells retain retinoid-laden lipid droplets after cellular transdifferentiation into activated myofibroblasts.American journal of physiology. Gastrointestinal and liver physiology · 2018Article
- Magnesium Isoglycyrrhizinate Ameliorates Fibrosis and Disrupts TGF-β-Mediated SMAD Pathway in Activated Hepatic Stellate Cell Line LX2.Frontiers in pharmacology · 2018Article
- Probiotics modify tight-junction proteins in an animal model of nonalcoholic fatty liver disease.Therapeutic advances in gastroenterology · 2016Article
- Role of Smad3 in platelet-derived growth factor-C-induced liver fibrosis.American journal of physiology. Cell physiology · 2016Article
- Involvement of TGF-β1/Smad3 Signaling in Carbon Tetrachloride-Induced Acute Liver Injury in Mice.PloS one · 2016Article
- Mapping the extracellular and membrane proteome associated with the vasculature and the stroma in the embryo.Molecular & cellular proteomics : MCP · 2013Article
- Translating an understanding of the pathogenesis of hepatic fibrosis to novel therapies.Clinical gastroenterology and hepatology : the official clinical practice journal of the American Gastroenterological Association · 2013Review
- Smooth muscle α actin (Acta2) and myofibroblast function during hepatic wound healing.PloS one · 2013Article
- Ingredients of Huangqi decoction slow biliary fibrosis progression by inhibiting the activation of the transforming growth factor-beta signaling pathway.BMC complementary and alternative medicine · 2012Article
- Endothelin and hepatic wound healing.Pharmacological research · 2011Review
- Modulation of hepatic fibrosis by c-Jun-N-terminal kinase inhibition.Gastroenterology · 2010Article
Corrections and comments
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Authors and funding
3 authors at 3 institutions in 1 country.
Funding
Abstract
In liver wound healing, transforming growth factor-beta (TGF-beta) plays a critical role in stellate cell activation as well as signaling cascades in the fibrogenic response to injury. We postulate that the TGF-beta-dependent downstream signaling pathway may vary according to the mechanism of stellate cell activation; this study was undertaken to ascertain whether the downstream signaling pathways mediated by TGF-beta vary in different liver injury models. We measured Smad3 and MAP kinase activation after isolating stellate cells from rat livers injured by either bile duct ligation (BDL) or repeated carbon tetrachloride (CCl(4)) administration. Phospho-Smad3 was dramatically up-regulated in stellate cells after CCl(4) injury, but not after BDL-induced injury. TGF-beta signaling in stellate cells activated after BDL was mediated prominently through ERK activation, whereas activation induced by CCl(4) injury or culture led to a cross-signaling mechanism involving both Smad3 and p38. The divergent Smad signaling pathways observed appeared to be attributable to the differential regulation of the early growth response gene-1 (Egr-1), an apparent negative transcriptional factor for Smad3 in our system. In addition, inhibition of ERK activation in stellate cells from BDL-injured liver led to a decrease in expression of endothelin-converting enzyme-1, a critical regulator of endothelin-1. We speculate that TGF-beta signaling proceeds through differential signaling pathways depending on the mechanism of liver injury that leads to stellate cell activation.
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