ArticleThe American journal of pathology2010
Disparate cellular basis of improved liver repair in beta-catenin-overexpressing mice after long-term exposure to 3,5-diethoxycarbonyl-1,4-dihydrocollidine.
Article in The American journal of pathology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Liver Progenitor Cells: Cellular Origins, Plasticity, and Signaling Pathways in Liver Regeneration.Biology · 2025Review
- Portal Fibrosis and the Ductular Reaction: Pathophysiological Role in the Progression of Liver Disease and Translational Opportunities.Gastroenterology · 2025Review
- Structural and functional effects of phosphopriming and scaffolding in the kinase GSK-3β.Science signaling · 2024Article
- Review
- Distinct hepatocyte identities in liver homeostasis and regeneration.JHEP reports : innovation in hepatology · 2023Review
- Atypical cholangiocytes derived from hepatocyte-cholangiocyte transdifferentiation mediated by COX-2: a kind of misguided liver regeneration.Inflammation and regeneration · 2023Article
- Small molecule drugs promote repopulation of transplanted hepatocytes by stimulating cell dedifferentiation.JHEP reports : innovation in hepatology · 2023Article
- Human menstrual blood-derived stem cell transplantation suppresses liver injury in DDC-induced chronic cholestasis.Stem cell research & therapy · 2022Article
- WNT7B Regulates Cholangiocyte Proliferation and Function During Murine Cholestasis.Hepatology communications · 2021Article
- The Thyromimetic Sobetirome (GC-1) Alters Bile Acid Metabolism in a Mouse Model of Hepatic Cholestasis.The American journal of pathology · 2020Article
- Liver Progenitors and Adult Cell Plasticity in Hepatic Injury and Repair: Knowns and Unknowns.Annual review of pathology · 2020Review
- Wnt-β-catenin signalling in liver development, health and disease.Nature reviews. Gastroenterology & hepatology · 2019Review
- YAP triggers the Wnt/β-catenin signalling pathway and promotes enterocyte self-renewal, regeneration and tumorigenesis after DSS-induced injury.Cell death & disease · 2018Article
- Wnt/β-Catenin Signaling in Liver Development, Homeostasis, and Pathobiology.Annual review of pathology · 2018Review
- Immortalized common marmoset (Cell discovery · 2018Article
- Wnt signaling regulates hepatobiliary repair following cholestatic liver injury in mice.Hepatology (Baltimore, Md.) · 2016Article
- Rb and p53 Liver Functions Are Essential for Xenobiotic Metabolism and Tumor Suppression.PloS one · 2016Article
- Deletion of Wntless in myeloid cells exacerbates liver fibrosis and the ductular reaction in chronic liver injury.Fibrogenesis & tissue repair · 2015Article
- Fibroblast growth factor signaling regulates the expansion of A6-expressing hepatocytes in association with AKT-dependent β-catenin activation.Journal of hepatology · 2014Article
- Sry HMG box protein 9-positive (Sox9+) epithelial cell adhesion molecule-negative (EpCAM-) biphenotypic cells derived from hepatocytes are involved in mouse liver regeneration.The Journal of biological chemistry · 2014Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Administration of a hepatotoxic diet containing 0.1% 3,5-diethoxycarbonyl-1,4-dihydrocollidine (DDC) induces biliary damage followed by hepatocyte injury, which is repaired through atypical ductular proliferation and oval cells and their subsequent differentiation to bile duct cells and hepatocytes. In this study, we examine whether excess β-catenin in transgenic (TG) mice would provide any reparative advantage in response to DDC. No differences in appearance or numbers of total A6-positive oval cells were observed after DDC administration. However, an increase in A6-positive "atypical hepatocytes" in the TG livers was observed after 14 and 28 days, coinciding with an increase in proliferating cell nuclear antigen-positive hepatocytes. Intriguingly, after chronic DDC administration for 150 days, a further increase in atypical hepatocytes was evident in TG mice, with higher numbers of proliferating cell nuclear antigen-positive hepatocytes exhibiting cytoplasmic/nuclear β-catenin and α-fetoprotein but not CK19, HNF1β, or Trop-2. Coincidently, we observed an improvement in intrahepatic cholestasis as seen by decreases in both serum bilirubin and alkaline phosphatase levels in TG mice, indicating an overall improvement in hepatic repair. TG mice exposed to DDC for 4 weeks followed by 2 days of normal chow showed decreases in alkaline phosphatase, atypical ductular proliferation, and periportal inflammation compared with wild-type animals, verifying improved biliary repair in TG livers. Thus, we report a potential role of β-catenin in liver repair, especially in enhancing the resolution of intrahepatic cholestasis after DDC injury.
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