ArticleProceedings of the National Academy of Sciences of the United States of America1999
Epidermal growth factor system regulates mucin production in airways.
Article in Proceedings of the National Academy of Sciences of the United States of America, 1999. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 186 papers.
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Who cites it
186 citing papers in PubMed, 580 citations in OpenAlex.
- Review
- Recent Progress in Treating Airway Mucus Hypersecretion by Targeting the Epidermal Growth Factor Receptor Signaling Pathway.Pediatric discovery · 2026Review
- How Does Biological Sex Impact Mucosal Bacterial Infection? Mucosal Defenses and Bacterial Detection.Immunological reviews · 2026Review
- Pharmacological Gq targeting prevents asthmatic airway remodeling.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- Taxifolin Regulates the Gene Expression of MUC5AC Mucin via Affecting IκBα/NF-κB p65 Signaling in Human Airway Epithelial Cells.Biomolecules & therapeutics · 2025Article
- Inflammatory Effects of Particulate Matter Exposure on the Nasal and Paranasal Sinus Mucosa in Rats.International journal of molecular sciences · 2025Article
- Development and Characterization of a Primary Ciliated Porcine Airway Model for the Evaluation of In Vitro Mucociliary Clearance and Mucosal Drug Delivery.Pharmaceutics · 2025Article
- Galangin Regulates Mucin 5AC Gene Expression via the Nuclear Factor-κB Inhibitor α/Nuclear Factor-κB p65 Pathway in Human Airway Epithelial Cells.Biomolecules & therapeutics · 2025Article
- Modulation of pulmonary immune functions by theFrontiers in immunology · 2025Review
- Airway epithelial cell-specific deletion of EGFR modulates mucoinflammatory features of cystic fibrosis-like lung disease in mice.Frontiers in immunology · 2025Article
- Effective-Component Compatibility of Bufei Yishen Formula (ECC-BYF) III Inhibits Mucus Hypersecretion by BEAS-2B Cells via miR-146a-5p-Mediated Regulation of the EGFR/MEK/ERK Pathway.International journal of chronic obstructive pulmonary disease · 2025Article
- Pyronaridine InhibitedBiomolecules & therapeutics · 2024Article
- Emerging cell and molecular targets for treating mucus hypersecretion in asthma.Allergology international : official journal of the Japanese Society of Allergology · 2024Review
- Submandibular Gland Pathogenesis Following SARS-CoV-2 Infection and Implications for Xerostomia.International journal of molecular sciences · 2024Article
- In vitro modelling of bacterial pneumonia: a comparative analysis of widely applied complex cell culture models.FEMS microbiology reviews · 2024Review
- Surfactant protein D prevents mucin overproduction in airway goblet cells via SIRPα.Scientific reports · 2024Article
- Localization of Sites of Osimertinib Action in Rat Intestine, Skin, and Lung by Immunohistochemistry.Acta histochemica et cytochemica · 2023Article
- Mucus hypersecretion in chronic obstructive pulmonary disease: From molecular mechanisms to treatment.Journal of translational internal medicine · 2023Article
- Regulation of the Gene Expression of Airway MUC5AC Mucin through NF-κB Signaling Pathway by Artesunate, an Antimalarial Agent.Biomolecules & therapeutics · 2023Article
- A human model of asthma exacerbation reveals transcriptional programs and cell circuits specific to allergic asthma.Science immunology · 2023Article
126 more citing papers are in PubMed but not listed here.
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Goblet-cell hyperplasia is a critical pathological feature in hypersecretory diseases of airways. However, the underlying mechanisms are unknown, and no effective therapy exists. Here we show that stimulation of epidermal growth factor receptors (EGF-R) by its ligands, EGF and transforming growth factor alpha (TGFalpha), causes MUC5AC expression in airway epithelial cells both in in vitro and in vivo. We found that a MUC5AC-inducing epithelial cell line, NCI-H292, expresses EGF-R constitutively; EGF-R gene expression was stimulated further by tumor necrosis factor alpha (TNFalpha). EGF-R ligands increased the expression of MUC5AC at both gene and protein levels, and this effect was potentiated by TNFalpha. Selective EGF-R tyrosine kinase inhibitors blocked MUC5AC expression induced by EGF-R ligands. Pathogen-free rats expressed little EGF-R protein in airway epithelial cells; intratracheal instillation of TNFalpha induced EGF-R in airway epithelial cells, and subsequent instillation of EGF-R ligands increased the number of goblet cells, Alcian blue-periodic acid-Schiff staining (reflecting mucous glycoconjugates), and MUC5AC gene expression, whereas TNFalpha, EGF, or TGFalpha alone was without effect. In sensitized rats, three intratracheal instillations of ovalbumin resulted in EGF-R expression and goblet-cell production in airway epithelium. Pretreatment with EGF-R tyrosine kinase inhibitor, BIBX1522, prevented goblet-cell production both in rats stimulated by TNFalpha-EGF-R ligands and in an asthma model. These findings suggest potential roles for inhibitors of the EGF-R cascade in hypersecretory diseases of airways.
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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.