ArticleAmerican journal of physiology. Lung cellular and molecular physiology2020
MUC1 contributes to goblet cell metaplasia and MUC5AC expression in response to cigarette smoke in vivo.
Article in American journal of physiology. Lung cellular and molecular physiology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers, 1 of them a synthesis that pooled it.
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Who cites it
22 citing papers in PubMed, 1 synthesis or guideline pooled it, 32 citations in OpenAlex.
- Roles of Exosomes in Chronic Rhinosinusitis: A Systematic Review.International journal of molecular sciences · 2022Pooled it
- Temporal Effects of Cigarette Smoke and Phytochemical-Based E-Liquid Aerosols on Tracheo-Alveolar Histopathology and the IL-6/TNF-α Molecular Signaling Axis.Current issues in molecular biology · 2026Article
- Epigenetic Dysregulation of the NKX2-1/SPDEF Axis Drives Persistent Goblet Cell Differentiation and Epithelial Barrier Dysfunction in Chronic Obstructive Pulmonary Disease.Respirology (Carlton, Vic.) · 2026Article
- The predictive value of MUC5AC levels in the sputum of children withMicrobiology spectrum · 2025Article
- Lung organoids in COPD: recent advances and future prospects.Respiratory research · 2025Review
- Diagnostic Challenges and Pathogenetic Differences in Biomass-Smoke-Induced versus Tobacco-Smoke-Induced COPD: A Comparative Review.Diagnostics (Basel, Switzerland) · 2024Review
- Chemical profiling and mechanisms of Agarikon pill in a rat model of cigarette smoke-induced chronic obstructive pulmonary disease.Journal of traditional and complementary medicine · 2024Article
- Molecular Mechanisms of N-Acetylcysteine in RSV Infections and Air Pollution-Induced Alterations: A Scoping Review.International journal of molecular sciences · 2024Article
- Mucins 3A and 3B Are Expressed in the Epithelium of Human Large Airway.International journal of molecular sciences · 2023Observational
- Steric pressure between glycosylated transmembrane proteins inhibits internalization by endocytosis.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Basic Science Perspective on Engineering and Modeling the Large Airways.Advances in experimental medicine and biology · 2023Article
- Physiology and pathophysiology of human airway mucus.Physiological reviews · 2022Review
- Immunological Aspects of Chronic Rhinosinusitis.Diagnostics (Basel, Switzerland) · 2022Review
- Article
- CTNNAL1 participates in the regulation of mucus overproduction in HDM-induced asthma mouse model through the YAP-ROCK2 pathway.Journal of cellular and molecular medicine · 2022Article
- Tumor necrosis factor-α promotes airway mucus hypersecretion by repressing miR-146a-5p and miR-134-5p levels in human airway epithelial cells.Translational cancer research · 2021Article
- The role of mucin 1 in respiratory diseases.European respiratory review : an official journal of the European Respiratory Society · 2021Review
- Emerging Biological Functions of IL-17A: A New Target in Chronic Obstructive Pulmonary Disease?Frontiers in pharmacology · 2021Review
- Influence of Hypoxia on the Epithelial-Pathogen Interactions in the Lung: Implications for Respiratory Disease.Frontiers in immunology · 2021Review
- A High-Content Screen for Mucin-1-Reducing Compounds Identifies Fostamatinib as a Candidate for Rapid Repurposing for Acute Lung Injury.Cell reports. Medicine · 2020Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Goblet cell metaplasia (GCM) and mucin overproduction are a hallmark of chronic rhinosinusitis (CRS) and chronic obstructive pulmonary disease (COPD). In the airways, cigarette smoke (CS) induces activation of the epidermal growth factor receptor (EGFR) leading to GCM and overexpression of the gel-forming mucin MUC5AC. Although previous studies have demonstrated that a membrane-bound mucin, MUC1, modulates the activation of CS-induced EGFR, the role of MUC1 in CS-induced GCM and mucin overproduction has not been explored. In response to CS exposure, wild-type (WT) rats displayed Muc1 translocation from the apical surface of airway epithelium to the intracellular compartment of hyperplastic intermediate cells, EGFR phosphorylation, GCM, and Muc5ac overproduction. Similarly, human CRS sinonasal tissues demonstrated hyperplasia of intermediate cells enriched with MUC1 in the intracellular compartment, which was accompanied by GCM and increased MUC5AC expression. To further evaluate the role of Muc1 in vivo, a Muc1 knockout (KO) rat (MUC in humans and Muc in animals) was developed. In contrast to WT littermates, Muc1-KO rats exhibited no activation of EGFR, and were protected from GCM and Muc5ac overproduction. Genetic knockdown of MUC1 in human lung or Muc1 knockout in primary rat airway epithelial cells led to significantly diminished EGF-induced MUC5AC production. Together, these findings suggest that MUC1-dependent EGFR activation mediates CS-induced GCM and mucin overproduction. Strategies designed to suppress MUC1-dependent EGFR activation may provide a novel therapeutic approach for treating mucin hypersecretion in CRS and COPD.
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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.