ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2016
Role of TGF-β signaling in differentiation of mesothelial cells to vitamin A-poor hepatic stellate cells in liver fibrosis.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 29 citations in OpenAlex.
- A mesothelial differentiation gateway drives fibrosis.Nature communications · 2025Article
- Bile acid regulation of xenobiotic nuclear receptors on the expressions of orosomucoids in the liver.American journal of physiology. Endocrinology and metabolism · 2025Article
- Low- and High-Grade Glioma-Associated Vascular Cells Differentially Regulate Tumor Growth.Molecular cancer research : MCR · 2024Article
- Regulation of Mesothelial Cell Fate during Development and Human Diseases.International journal of molecular sciences · 2022Review
- DOCK2 Promotes Pleural Fibrosis by Modulating Mesothelial to Mesenchymal Transition.American journal of respiratory cell and molecular biology · 2022Article
- Research Progress of Fibroblast Growth Factor 21 in Fibrotic Diseases.Oxidative medicine and cellular longevity · 2022Review
- Identification of growth differentiation factor 15 as a pro-fibrotic factor in mouse liver fibrosis progression.International journal of experimental pathology · 2021Article
- Sectm1a Facilitates Protection against Inflammation-Induced Organ Damage through Promoting TRM Self-Renewal.Molecular therapy : the journal of the American Society of Gene Therapy · 2021Article
- Cellular Mechanisms of Liver Fibrosis.Frontiers in pharmacology · 2021Review
- Candidate rejuvenating factor GDF11 and tissue fibrosis: friend or foe?GeroScience · 2020Review
- Development of Capsular Fibrosis Beneath the Liver Surface in Humans and Mice.Hepatology (Baltimore, Md.) · 2020Article
- Review
- Crosstalk network among multiple inflammatory mediators in liver fibrosis.World journal of gastroenterology · 2019Review
- Study of the mechanism underlying hsa-miR338-3p downregulation to promote fibrosis of the synovial tissue in osteoarthritis patients.Molecular biology reports · 2019Article
- Blocking follistatin-like 1 attenuates liver fibrosis in mice by regulating transforming growth factor-beta signaling.International journal of clinical and experimental pathology · 2018Article
- Genomic reprograming analysis of the Mesothelial to Mesenchymal Transition identifies biomarkers in peritoneal dialysis patients.Scientific reports · 2017Article
- MircoRNA-145 promotes activation of hepatic stellate cells via targeting krüppel-like factor 4.Scientific reports · 2017Article
- Construction of Gpm6a/ReelinWorld journal of gastroenterology · 2017Article
- Characterization of hepatic stellate cells, portal fibroblasts, and mesothelial cells in normal and fibrotic livers.Journal of hepatology · 2016Article
- The Role of Mesothelial Cells in Liver Development, Injury, and Regeneration.Gut and liver · 2016Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Mesothelial cells (MCs) form a single layer of the mesothelium and cover the liver surface. A previous study demonstrated that, upon liver injury, MCs migrate inward from the liver surface and give rise to hepatic stellate cells (HSCs) in biliary fibrosis induced by bile duct ligation (BDL) or myofibroblasts in CCl4-induced fibrosis. The present study analyzed the role of transforming growth factor-β (TGF-β) signaling in mesothelial-mesenchymal transition (MMT) and the fate of MCs during liver fibrosis and its regression. Deletion of TGF-β type II receptor (Tgfbr2) gene in cultured MCs suppressed TGF-β-mediated myofibroblastic conversion. Conditional deletion of Tgfbr2 gene in MCs reduced the differentiation of MCs to HSCs and myofibroblasts in the BDL and CCl4 models, respectively, indicating that the direct TGF-β signaling in MCs is responsible to MMT. After BDL and CCl4 treatment, MC-derived HSCs and myofibroblasts were distributed near the liver surface and the thickness of collagen was increased in Glisson's capsule beneath the liver surface. Fluorescence-activated cell sorting analysis revealed that MC-derived HSCs and myofibroblasts store little vitamin A lipids and have fibrogenic phenotype in the fibrotic livers. MCs contributed to 1.4 and 2.0% of activated HSCs in the BDL and CCl4 models, respectively. During regression of CCl4-induced fibrosis, 20% of MC-derived myofibroblasts survived in the liver and deactivated to vitamin A-poor HSCs. Our data indicate that MCs participate in capsular fibrosis by supplying vitamin A-poor HSCs during a process of liver fibrosis and regression.
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