ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2015
Loss of hepatocyte EGFR has no effect alone but exacerbates carbon tetrachloride-induced liver injury and impairs regeneration in hepatocyte Met-deficient mice.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Hepatocyte-specific epidermal growth factor receptor (EGFR) deletion attenuates acetaminophen-induced liver injury in mice.Toxicological sciences : an official journal of the Society of Toxicology · 2026Article
- Potential role of epidermal growth factor receptors (EGFR) signaling in the pathogenesis and management of hepatocellular carcinoma.BioImpacts : BI · 2025Review
- Three Dimensional Bioprinting for Hepatic Tissue Engineering: From In Vitro Models to Clinical Applications.Tissue engineering and regenerative medicine · 2024Review
- EGF-receptor phosphorylation and downstream signaling are activated by genistein during subacute liver damage.Journal of molecular histology · 2023Article
- Unveiling the power of microenvironment in liver regeneration: an in-depth overview.Frontiers in genetics · 2023Review
- The application of cytokeratin-18 as a biomarker for drug-induced liver injury.Archives of toxicology · 2021Review
- ADAM10 and ADAM17 regulate EGFR, c-Met and TNF RI signalling in liver regeneration and fibrosis.Scientific reports · 2021Article
- Liver regeneration: biological and pathological mechanisms and implications.Nature reviews. Gastroenterology & hepatology · 2021Review
- Bone morphogenetic protein 8B promotes the progression of non-alcoholic steatohepatitis.Nature metabolism · 2020Article
- Mechanisms and biomarkers of liver regeneration after drug-induced liver injury.Advances in pharmacology (San Diego, Calif.) · 2019Review
- Lipin deactivation after acetaminophen overdose causes phosphatidic acid accumulation in liver and plasma in mice and humans and enhances liver regeneration.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018Article
- Epidermal Growth Factor Receptor Signaling Disruption by Endocrine and Metabolic Disrupting Chemicals.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Polychlorinated biphenyls disrupt hepatic epidermal growth factor receptor signaling.Xenobiotica; the fate of foreign compounds in biological systems · 2017Article
- Ductular reaction correlates with fibrogenesis but does not contribute to liver regeneration in experimental fibrosis models.PloS one · 2017Article
- Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- Combined systemic elimination of MET and epidermal growth factor receptor signaling completely abolishes liver regeneration and leads to liver decompensation.Hepatology (Baltimore, Md.) · 2016Article
- EGFR Signaling in Liver Diseases.International journal of molecular sciences · 2015Review
- Loss of hepatocyte ERBB3 but not EGFR impairs hepatocarcinogenesis.American journal of physiology. Gastrointestinal and liver physiology · 2015Article
- Transgenic expression of the human growth hormone minigene promotes pancreatic β-cell proliferation.American journal of physiology. Regulatory, integrative and comparative physiology · 2015Article
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Authors and funding
5 authors.
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Abstract
The role(s) of the epidermal growth factor receptor (EGFR) in hepatocytes is unknown. We generated a murine hepatocyte specific-EGFR knockout (KO) model to evaluate how loss of hepatocellular EGFR expression affects processes such as EGF clearance, circulating EGF concentrations, and liver regeneration following 70% resection or CCl4-induced centrilobular injury. We were able to disrupt EGFR expression effectively in hepatocytes and showed that the ability of EGF and heregulin (HRG) to phosphorylate EGFR and ERBB3, respectively, required EGFR. Loss of hepatocellular EGFR impaired clearance of exogenous EGF from the portal circulation but paradoxically resulted in reduced circulating levels of endogenous EGF. This was associated with decreased submandibular salivary gland production of EGF. EGFR disruption did not result in increased expression of other ERBB proteins or Met, except in neonatal mice. Liver regeneration following 70% hepatectomy revealed a mild phenotype, with no change in cyclin D1 expression and slight differences in cyclin A expression compared with controls. Peak 5-bromo-2'-deoxyuridine labeling was shifted from 36 to 48 h. Centrilobular damage and regenerative response induced by carbon tetrachloride (CCl4) were identical in the KO and wild-type mice. In contrast, loss of Met increased CCl4-induced necrosis and delayed regeneration. Although loss of hepatocellular EGFR alone did not have an effect in this model, EGFR-Met double KOs displayed enhanced necrosis and delayed liver regeneration compared with Met KOs alone. This suggests that EGFR and Met may partially compensate for the loss of the other, although other compensatory mechanisms can be envisioned.
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