ArticleThe American journal of pathology2005
Growth inhibition and apoptosis in liver myofibroblasts promoted by hepatocyte growth factor leads to resolution from liver cirrhosis.
Article in The American journal of pathology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed.
- Hepatocyte-hepatic stellate cell interactions in liver fibrosis: Mechanisms and therapeutic implications.Hepatology communications · 2026Review
- Targeting chronic liver diseases: Molecular markers, drug delivery strategies and future perspectives.International journal of pharmaceutics · 2024Review
- Article
- Review
- Platelets in Non-alcoholic Fatty Liver Disease.Frontiers in pharmacology · 2022Review
- ATP Secretion and Metabolism in Regulating Pancreatic Beta Cell Functions and Hepatic Glycolipid Metabolism.Frontiers in physiology · 2022Review
- Till Death Do Us Part-The Multifaceted Role of Platelets in Liver Diseases.International journal of molecular sciences · 2021Review
- Platelets in chronic liver disease, from bench to bedside.JHEP reports : innovation in hepatology · 2019Review
- Human umbilical cord mesenchymal stem cells inhibit proliferation of hepatic stellate cells in vitro.International journal of molecular medicine · 2018Article
- Novel Combination BMP7 and HGF Gene Therapy Instigates Selective Myofibroblast Apoptosis and Reduces Corneal Haze In Vivo.Investigative ophthalmology & visual science · 2018Article
- The role of hepatocyte growth factor in corneal wound healing.Experimental eye research · 2018Review
- Effect of Yi Guan Jian decoction on differentiation of bone marrow mesenchymalstem cells into hepatocyte-like cells in dimethylnitrosamine-induced liver cirrhosis in mice.Molecular medicine reports · 2017Article
- The roles of microRNA families in hepatic fibrosis.Cell & bioscience · 2017Review
- Multifaceted Therapeutic Benefits of Factors Derived From Dental Pulp Stem Cells for Mouse Liver Fibrosis.Stem cells translational medicine · 2016Article
- M10, a caspase cleavage product of the hepatocyte growth factor receptor, interacts with Smad2 and demonstrates antifibrotic properties in vitro and in vivo.Translational research : the journal of laboratory and clinical medicine · 2016Article
- Clinical Advancements in the Targeted Therapies against Liver Fibrosis.Mediators of inflammation · 2016Review
- Pharmacological Intervention in Hepatic Stellate Cell Activation and Hepatic Fibrosis.Frontiers in pharmacology · 2016Review
- BCL6B expression in hepatocellular carcinoma and its efficacy in the inhibition of liver damage and fibrogenesis.Oncotarget · 2015Article
- Inhibition of hepatic stellate cells by bone marrow-derived mesenchymal stem cells in hepatic fibrosis.Clinical and molecular hepatology · 2015Article
- Deletion of Wntless in myeloid cells exacerbates liver fibrosis and the ductular reaction in chronic liver injury.Fibrogenesis & tissue repair · 2015Article
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Liver cirrhosis is characterized by hepatic dysfunction with extensive accumulation of fibrous tissue in the liver. In response to chronic hepatic injury, hepatic portal myofibroblasts and activated hepatic stellate cells (HSCs) play a role in liver fibrosis. Although administration or gene expression of hepatocyte growth factor (HGF) leads to improvement in hepatic fibrosis/cirrhosis, the related mechanisms are not fully understood. We investigated mechanisms involved in resolution from liver cirrhosis by HGF, focusing on growth regulation and apoptosis in portal myofibroblasts. Cultured rat HSCs could not proliferate, were withdrawn after passage, and were replaced by proliferating portal myofibroblasts during the passages. In quiescent HSCs, c-Met receptor expression was undetected whereas c-Met receptor expression was detected in activated HSCs and liver myofibroblasts expressing alpha-smooth muscle actin (alpha-SMA), suggesting that activated HSCs and portal myofibroblasts are targets of HGF. For cultured rat portal myofibroblasts, HGF counteracted phosphorylation of extracellular signal-regulated kinase (Erk) 1/2 and mitogenic stimulus induced by platelet-derived growth factor, induced c-jun N-terminal kinase (JNK) 1 phosphorylation, and promoted apoptotic cell death. In the dimethylnitrosamine rat model of liver cirrhosis, administration of HGF suppressed proliferation while promoting apoptosis of alpha-SMA-positive cells in the liver, events that were associated with reduced hepatic expressions of alpha-SMA and histological resolution from liver cirrhosis. Growth inhibition and enhanced apoptosis in portal myofibroblasts by HGF are newly identified mechanisms aiding resolution from liver fibrosis/cirrhosis by HGF.
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