ArticleThe American journal of pathology2006
MUC5AC, a gel-forming mucin accumulating in gallstone disease, is overproduced via an epidermal growth factor receptor pathway in the human gallbladder.
Article in The American journal of pathology, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 66 citations in OpenAlex.
- Shared molecular mechanisms of common differentially expressed genes (C-DEGs) linking gallbladder stones to carcinogenesis: integrated bioinformatics and experimental validation.Cancer cell international · 2026Article
- Biological relationship between Parkinson's disease and gallstone disease.Neuroprotection (Chichester, England) · 2025Review
- Polydatin prevents cholesterol gallstone formation by regulating cholesterol metabolism via PPAR-γ signaling.Open life sciences · 2025Article
- Identification of Gallbladder-Specific Distal Regulatory Sequence of Murine Sox17.Genes to cells : devoted to molecular & cellular mechanisms · 2025Article
- Review
- Immunohistochemical detection of MUC5AC and MUC5B mucins in ferrets.BMC research notes · 2023Article
- Adeno-associated virus-based caveolin-1 delivery via different routes for the prevention of cholesterol gallstone formation.Lipids in health and disease · 2022Article
- Research progress on the immune microenvironment of the gallbladder in patients with cholesterol gallstones.World journal of gastrointestinal surgery · 2022Review
- MUC Expression in Gallbladder Epithelial Tissues in Cholesterol-Associated Gallbladder Disease.Gut and liver · 2016Article
- Article
- Cholesterol gallstone disease: focusing on the role of gallbladder.Laboratory investigation; a journal of technical methods and pathology · 2015Review
- Article
- A genetic model for gallbladder carcinogenesis and its dissemination.Annals of oncology : official journal of the European Society for Medical Oncology · 2014Review
- Cytokine single nucleotide polymorphisms in patients' with gallstone: dose TGF-β gene variants affect gallstone formation?Molecular biology reports · 2013Article
- Gallbladder epithelium as a niche for chronic Salmonella carriage.Infection and immunity · 2013Article
- LPS increases MUC5AC by TACE/TGF-α/EGFR pathway in human intrahepatic biliary epithelial cell.BioMed research international · 2013Article
- A crucial role of Flagellin in the induction of airway mucus production by Pseudomonas aeruginosa.PloS one · 2012Article
- Steatocholecystitis and fatty gallbladder disease.Digestive diseases and sciences · 2009Review
- Roles of infection, inflammation, and the immune system in cholesterol gallstone formation.Gastroenterology · 2009Review
- Steatocholecystitis: the influence of obesity and dietary carbohydrates.The Journal of surgical research · 2008Article
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Authors and funding
11 authors at 6 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite evidence that mucin overproduction is critical in the pathogenesis of gallstones, the mechanisms triggering mucin production in gallstone disease are unknown. Here, we tested the potential implication of an inflammation-dependent epidermal growth factor receptor (EGF-R) pathway in the regulation of gallbladder mucin synthesis. In gallbladder tissue sections from subjects with cholesterol gallstones, mucus accumulation was associated with neutrophil infiltration and with increased expressions of EGF-R and of tumor necrosis factor-alpha (TNF-alpha). In primary cultures of human gallbladder epithelial cells, TNF-alpha induced EGF-R overexpression. In the presence of TNF-alpha, EGF-R ligands (either EGF or transforming growth factor-alpha) caused significant increases in MUC5AC mRNA and protein production, whereas expression of the other gallbladder mucins MUC1, MUC3, and MUC5B was unchanged. In addition, on gallbladder tissue sections from subjects with gallstones, increased MUC5AC immunoreactivity was detected in the epithelium and within mucus gel in the lumen. Studies in primary cultures demonstrated that MUC5AC up-regulation induced by the combination of TNF-alpha with EGF-R ligands was completely blunted by inhibitors of EGF-R tyrosine kinase and mitogen-activated protein/extracellular signal-related kinase kinase. In conclusion, an inflammation-dependent EGF-R cascade causes overproduction of the gel-forming mucin MUC5AC, which accumulates in cholesterol gallstone disease. The ability to interrupt this cascade is of potential interest in the prevention of cholesterol gallstones.
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