ArticleHistochemistry and cell biology2010
Phenotype and growth behavior of residual β-catenin-positive hepatocytes in livers of β-catenin-deficient mice.
Article in Histochemistry and cell biology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 38 citations in OpenAlex.
- Cytochrome P450 enzymes as modulators of oncogenic signaling via the Wnt/β-catenin signaling pathway.Archives of toxicology · 2026Review
- The potent human CAR activator CITCO is a non-genotoxic hepatic tumour-promoting agent in humanised constitutive androstane receptor mice but not in wild-type animals.Archives of toxicology · 2025Article
- β-catenin signaling, the constitutive androstane receptor and their mutual interactions.Archives of toxicology · 2020Review
- Amniotic mesenchymal stem cells derived hepatocyte-like cells attenuated liver fibrosis more efficiently by mixed-cell transplantation.International journal of physiology, pathophysiology and pharmacology · 2020Article
- Article
- Signal integration by the CYP1A1 promoter--a quantitative study.Nucleic acids research · 2015Article
- Highlight report: Software for tissue analysis and reconstruction.EXCLI journal · 2015Article
- Genetic ablation of β-catenin inhibits the proliferative phenotype of mouse liver adenomas.British journal of cancer · 2014Article
- Protocols for staining of bile canalicular and sinusoidal networks of human, mouse and pig livers, three-dimensional reconstruction and quantification of tissue microarchitecture by image processing and analysis.Archives of toxicology · 2014Article
- Quantification of three-dimensional structures in liver tissue: bile canalicular and sinusoidal networks.EXCLI journal · 2014Article
- A novel role of nucleostemin in maintaining the genome integrity of dividing hepatocytes during mouse liver development and regeneration.Hepatology (Baltimore, Md.) · 2013Article
- Recent advances in 2D and 3D in vitro systems using primary hepatocytes, alternative hepatocyte sources and non-parenchymal liver cells and their use in investigating mechanisms of hepatotoxicity, cell signaling and ADME.Archives of toxicology · 2013Review
- Postnatal development, maturation and aging in the mouse cochlea and their effects on hair cell regeneration.Hearing research · 2013Review
- Advances in 2D and 3D in vitro systems for hepatotoxicity testing.EXCLI journal · 2013Article
- Pericentral activity of alpha-fetoprotein enhancer 3 and glutamine synthetase upstream enhancer in the adult liver are regulated by β-catenin in mice.Hepatology (Baltimore, Md.) · 2012Article
- Hepatocyte γ-catenin compensates for conditionally deleted β-catenin at adherens junctions.Journal of hepatology · 2011Article
- Depletion of β-catenin from mature hepatocytes of mice promotes expansion of hepatic progenitor cells and tumor development.Proceedings of the National Academy of Sciences of the United States of America · 2011Article
- Phenotype of single hepatocytes expressing an activated version of β-catenin in liver of transgenic mice.Journal of molecular histology · 2011Article
- Spontaneous repopulation of β-catenin null livers with β-catenin-positive hepatocytes after chronic murine liver injury.Hepatology (Baltimore, Md.) · 2011Article
- Histochemistry and cell biology: the annual review 2010.Histochemistry and cell biology · 2011Review
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Signaling through the Wnt/β-catenin pathway is a crucial determinant of hepatic zonal gene expression, liver development, regeneration, and tumorigenesis. Transgenic mice with hepatocyte-specific knockout of Ctnnb1 (encoding β-catenin) have proven their usefulness in elucidating these processes. We now found that a small number of hepatocytes escape the Cre-mediated gene knockout in that mouse model. The remaining β-catenin-positive hepatocytes showed approximately 25% higher cell volumes compared to the β-catenin-negative cells and exhibited a marker protein expression profile similar to that of normal perivenous hepatocytes or hepatoma cells with mutationally activated β-catenin. Surprisingly, the expression pattern was observed independent of the cell's position within the liver lobule, suggesting a malfunction of physiological periportal repression of perivenously expressed genes in β-catenin-deficient liver. Clusters of β-catenin-expressing hepatocytes lacked expression of the gap junction proteins Connexin 26 and 32. Nonetheless, β-catenin-positive hepatocytes had no striking proliferative advantage, but started to grow out on treatment with phenobarbital, a tumor-promoting agent known to facilitate the formation of mouse liver adenoma with activating mutations of Ctnnb1. Progressive re-population of Ctnnb1 knockout livers with wild-type hepatocytes was seen in aged mice with a pre-cirrhotic phenotype. In these large clusters of β-catenin-expressing hepatocytes, perivenous-specific gene expression was re-established. In summary, our data demonstrate that the zone-specificity of a hepatocyte's gene expression profile is dependent on the presence of β-catenin, and that β-catenin provides a proliferative advantage to hepatocytes when promoted with phenobarbital, or in a pre-cirrhotic environment.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.