ArticleThe Journal of physiology2012
Association of TMEM16A chloride channel overexpression with airway goblet cell metaplasia.
Article in The Journal of physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 100 papers.
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Who cites it
100 citing papers in PubMed, 161 citations in OpenAlex.
- Pseudomonas aeruginosa induces the generation of pathogenic IFNγNature microbiology · 2026Article
- TRPV4-driven ATP release activates CFTR through ADORA2B and P2RY2 receptors in the airway epithelium.iScience · 2026Article
- Quantitative characterisation of extracellular vesicles designed to decoy or compete with SARS-CoV-2 reveals differential mode of action across variants of concern and highlights the diversity of Omicron.Cell communication and signaling : CCS · 2025Article
- [Transmembrane protein 16A--a new target for the treatment of airway inflammatory diseases].Lin chuang er bi yan hou tou jing wai ke za zhi = Journal of clinical otorhinolaryngology head and neck surgery · 2025Review
- The apical mucus layer alters the pharmacological properties of the airway epithelium.The Journal of physiology · 2025Article
- Functional rescue of F508del-CFTR through revertant mutations introduced by CRISPR base editing.Molecular therapy : the journal of the American Society of Gene Therapy · 2025Article
- The Tmem16a chloride channel is required for mucin maturation after secretion from goblet-like cells in the Xenopus tropicalis tadpole skin.Scientific reports · 2024Article
- CoCas9 is a compact nuclease from the human microbiome for efficient and precise genome editing.Nature communications · 2024Article
- Inhibition of mucus secretion by niclosamide and benzbromarone in airways and intestine.Scientific reports · 2024Article
- Approach for Elucidating the Molecular Mechanism of Epithelial to Mesenchymal Transition in Fibrosis of Asthmatic Airway Remodeling Focusing on ClInternational journal of molecular sciences · 2023Review
- The Anion Channel TMEM16a/Ano1 Modulates CFTR Activity, but Does Not Function as an Apical Anion Channel in Colonic Epithelium from Cystic Fibrosis Patients and Healthy Individuals.International journal of molecular sciences · 2023Article
- Functional restoration of a CFTR splicing mutation through RNA delivery of CRISPR adenine base editor.Molecular therapy : the journal of the American Society of Gene Therapy · 2023Article
- Novel tricyclic pyrrolo-quinolines as pharmacological correctors of the mutant CFTR chloride channel.Scientific reports · 2023Article
- Easy-to-Build and Reusable Microfluidic Device for the Dynamic Culture of Human Bronchial Cystic Fibrosis Epithelia.ACS biomaterials science & engineering · 2023Article
- Pharmacological potentiators of the calcium signaling cascade identified by high-throughput screening.PNAS nexus · 2023Article
- Discovery of Fungus-Derived Nornidulin as a Novel TMEM16A Inhibitor: A Potential Therapy to Inhibit Mucus Secretion in Asthma.Journal of experimental pharmacology · 2023Article
- Article
- Airway surface hyperviscosity and defective mucociliary transport by IL-17/TNF-α are corrected by β-adrenergic stimulus.JCI insight · 2022Article
- Drug Repurposing for Cystic Fibrosis: Identification of Drugs That Induce CFTR-Independent Fluid Secretion in Nasal Organoids.International journal of molecular sciences · 2022Article
- Physiology and pathophysiology of human airway mucus.Physiological reviews · 2022Review
40 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on byTime for TMEM?2012
Authors and funding
13 authors at 2 institutions in 1 country.
Funding
Abstract
The TMEM16A protein has a potential role as a Ca(2+)-activated Cl(-) channel (CaCC) in airway epithelia where it may be important in the homeostasis of the airway surface fluid. We investigated the function and expression of TMEM16A in primary human bronchial epithelial cells and in a bronchial cell line (CFBE41o-). Under resting conditions, TMEM16A protein expression was relatively low. However, TMEM16A silencing with short-interfering RNAs caused a marked inhibition of CaCC activity, thus demonstrating that a low TMEM16A expression is sufficient to support Ca(2+)-dependent Cl(-) transport. Following treatment for 24-72 h with interleukin-4 (IL-4), a cytokine that induces mucous cell metaplasia, TMEM16A protein expression was strongly increased in approximately 50% of primary bronchial epithelial cells, with a specific localization in the apical membrane. IL-4 treatment also increased the percentage of cells expressing MUC5AC, a marker of goblet cells. Interestingly, MUC5AC was detected specifically in cells expressing TMEM16A. In particular, MUC5AC was found in 15 and 60% of TMEM16A-positive cells when epithelia were treated with IL-4 for 24 or 72 h, respectively. In contrast, ciliated cells showed expression of the cystic fibrosis transmembrane conductance regulator Cl(-) channel but not of TMEM16A. Our results indicate that TMEM16A protein is responsible for CaCC activity in airway epithelial cells, particularly in cells treated with IL-4, and that TMEM16A upregulation by IL-4 appears as an early event of goblet cell differentiation. These findings suggest that TMEM16A expression is particularly required under conditions of mucus hypersecretion to ensure adequate secretion of electrolytes and water.
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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.