ArticleLaboratory investigation; a journal of technical methods and pathology2012
Heparin-binding epidermal growth factor-like growth factor suppresses experimental liver fibrosis in mice.
Article in Laboratory investigation; a journal of technical methods and pathology, 2012. 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, 36 citations in OpenAlex.
- ADAM17 as a proteolytic rheostat linking inflammation, tissue repair, and failure of inflammatory resolution in liver injury and fibrosis.Frontiers in pharmacology · 2026Review
- Role of mitogens in normal and pathological liver regeneration.Hepatology communications · 2025Review
- Bioinformatics based exploration of the anti-liver fibrosis mechanism of Pien Tze Huang via EGFR/JAK1/STAT3 pathway.Frontiers in immunology · 2025Article
- Review
- Predictive Power of Tissue and Circulating Biomarkers for the Severity of Biopsy-Validated Chronic Liver Diseases.Journal of clinical medicine · 2022Article
- Paracrine HB-EGF signaling reduce enhanced contractile and energetic state of activated decidual fibroblasts by rebalancing SRF-MRTF-TCF transcriptional axis.Frontiers in cell and developmental biology · 2022Article
- Angiodiversity and organotypic functions of sinusoidal endothelial cells.Angiogenesis · 2021Review
- Role of Heparin-Binding Epidermal Growth Factor-Like Growth Factor in Oxidative Stress-Associated Metabolic Diseases.Metabolic syndrome and related disorders · 2020Review
- Review
- Soluble Heparin Binding Epidermal Growth Factor-Like Growth Factor Is a Regulator ofMolecular and cellular biology · 2019Article
- Heparin-binding EGF-like growth factor (HB-EGF) antisense oligonucleotide protected against hyperlipidemia-associated atherosclerosis.Nutrition, metabolism, and cardiovascular diseases : NMCD · 2019Article
- Incomplete Differentiation of Engrafted Bone Marrow Endothelial Progenitor Cells Initiates Hepatic Fibrosis in the Rat.Hepatology (Baltimore, Md.) · 2019Article
- The effect of HIV infection and HCV viremia on inflammatory mediators and hepatic injury-The Women's Interagency HIV Study.PloS one · 2017Article
- Article
- Heparin-binding epidermal growth factor-like growth factor and hepatocyte growth factor inhibit cholestatic liver injury in mice through different mechanisms.International journal of molecular medicine · 2016Article
- Hepatocyte ERBB3 and EGFR are required for maximal CCl4-induced liver fibrosis.American journal of physiology. Gastrointestinal and liver physiology · 2016Article
- The Characteristics Variation of Hepatic Progenitors after TGF-β1-Induced Transition and EGF-Induced Reversion.Stem cells international · 2016Article
- EGFR Signaling in Liver Diseases.International journal of molecular sciences · 2015Review
- Plumbagin Ameliorates CCl 4 -Induced Hepatic Fibrosis in Rats via the Epidermal Growth Factor Receptor Signaling Pathway.Evidence-based complementary and alternative medicine : eCAM · 2015Article
- Pathogenesis and prevention of hepatitis C virus-induced hepatocellular carcinoma.Journal of hepatology · 2014Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Heparin-binding epidermal growth factor-like growth factor (HB-EGF) is a cytoprotective agent in several organ systems but its roles in liver fibrosis are unclear. We studied the roles of HB-EGF in experimental liver fibrosis in mice and during hepatic stellate cell (HSC) activation. Thioacetamide (TAA; 100 mg/kg) was administered by intraperitoneal injection three times a week for 4 weeks to wild-type HB-EGF(+/+) or HB-EGF-null (HB-EGF(-/-)) male mice. Livers were examined for histology and expression of key fibrotic markers. Primary cultured HSCs isolated from untreated HB-EGF(+/+) or HB-EGF(-/-) mice were examined for fibrotic markers and/or cell migration either during culture-induced activation or after exogenous HB-EGF (100 ng/ml) treatment. TAA induced liver fibrosis in both HB-EGF(+/+) and HB-EGF(-/-) mice. Hepatic HB-EGF expression was decreased in TAA-treated HB-EGF(+/+) mice by 37.6% (P<0.05) as compared with animals receiving saline alone. HB-EGF(-/-) mice treated with TAA showed increased hepatic α-smooth muscle actin-positive cells and collagen deposition, and, as compared with HB-EGF(+/+) mice, TAA-stimulated hepatic mRNA levels in HB-EGF(-/-) mice were, respectively, 2.1-, 1.7-, 1.8-, 2.2-, 1.2- or 3.3-fold greater for α-smooth muscle actin, α1 chain of collagen I or III (COL1A1 or COL3A1), transforming growth factor-β1, connective tissue growth factor or tissue inhibitor of metalloproteinase-1 (P<0.05). HB-EGF expression was detectable in primary cultured HSCs from HB-EGF(+/+) mice. Both endogenous and exogenous HB-EGF inhibited HSC activation in primary culture, and HB-EGF enhanced HSC migration. These findings suggest that HB-EGF gene knockout in mice increases susceptibility to chronic TAA-induced hepatic fibrosis and that HB-EGF expression or action is associated with suppression of fibrogenic pathways in HSCs.
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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.