ArticleAmerican journal of respiratory cell and molecular biology2011
Prostaglandin E₂regulation of cystic fibrosis transmembrane conductance regulator activity and airway surface liquid volume requires gap junctional communication.
Article in American journal of respiratory cell and molecular biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Cx43 levels guide apicobasal polarity in regenerating airway epithelial cells.Communications biology · 2026Article
- Beyond the mutations: spatiotemporal regulation of CFTR by cAMP and calcium signaling in epithelial physiology and cystic fibrosis.Cellular & molecular biology letters · 2025Review
- Impact of overexpression of wild-type CFTR and elexacaftor-tezacaftor-ivacaftor on oxylipin production by the CFBE41o- bronchial epithelial cell line.Prostaglandins & other lipid mediators · 2025Article
- Ezrin Contributes to the Damage of Airway Epithelial Barrier Related to Diabetes Mellitus.Journal of inflammation research · 2024Article
- Shuttle peptide delivers base editor RNPs to rhesus monkey airway epithelial cells in vivo.Nature communications · 2023Article
- Dynamic regulation of airway surface liquid pH by TMEM16A and SLC26A4 in cystic fibrosis nasal epithelia with rare mutations.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Intercellular Communication in Airway Epithelial Cell Regeneration: Potential Roles of Connexins and Pannexins.International journal of molecular sciences · 2023Review
- SARS-CoV-2 viral entry and replication is impaired in Cystic Fibrosis airways due to ACE2 downregulation.Nature communications · 2023Article
- Increased CFTR expression and function from an optimized lentiviral vector for cystic fibrosis gene therapy.Molecular therapy. Methods & clinical development · 2021Article
- Gap Junctions Are Involved in the Rescue of CFTR-Dependent Chloride Efflux by Amniotic Mesenchymal Stem Cells in Coculture with Cystic Fibrosis CFBE41o- Cells.Stem cells international · 2018Article
- Secondhand Smoke-Prevalent Polycyclic Aromatic Hydrocarbon Binary Mixture-Induced Specific Mitogenic and Pro-inflammatory Cell Signaling Events in Lung Epithelial Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Mind the Gaps in Tumor Immunity: Impact of Connexin-Mediated Intercellular Connections.Frontiers in immunology · 2017Review
- Control of local immunity by airway epithelial cells.Mucosal immunology · 2016Review
- Junctional abnormalities in human airway epithelial cells expressing F508del CFTR.American journal of physiology. Lung cellular and molecular physiology · 2015Article
- The lung communication network.Cellular and molecular life sciences : CMLS · 2015Review
- An unexpected effect of TNF-α on F508del-CFTR maturation and function.F1000Research · 2015Article
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- Role of adenosine A(2B) receptors in inflammation.Advances in pharmacology (San Diego, Calif.) · 2011Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 3 countries.
Funding
Abstract
Stimulation of the cystic fibrosis transmembrane conductance regulator (CFTR) by protease-activated receptors (PARs) at the basolateral membranes and by adenosine receptors (ADO-Rs) at the apical membrane maintain airway surface liquid (ASL) volume, which is required to ensure hydrated and clearable mucus. Both pathways involve the release of prostaglandin E₂ (PGE₂) and the stimulation of their basolateral receptors (EP-Rs). We sought to determine whether gap junctions contribute to the coordination of these pathways for modulating CFTR activity and mucus hydration. We used RT-PCR and Western blotting to determine connexin (Cx), CD73, and EP-R expression in a Calu-3 airway epithelial cell line grown on Transwell (Corning Costar, Cambridge, MA) inserts. We used dye coupling to evaluate gap junctional intercellular communication (GJIC). We used Ussing chamber studies and X-Z confocal microscopy to monitor Cl(-) secretion and ASL volume regulation. We found that connexin 43 (Cx43)-mediated GJIC was increased either by endogenous ADO after the hydrolysis of purine nucleotides by CD73 or by the direct activation of ADO-Rs. Inhibition of phospholipase A2 and cyclooxygenase prevented ADO-dependent increases in GJIC, suggesting the involvement of PGE₂. PGE₂ was found to increase GJIC markedly by stimulating EP4-Rs. The modulation of ADO signaling also affected the PAR-dependent activation of CFTR. The reduction of GJIC by CD73 or Cx43 inhibition prevented PAR-evoked CFTR currents in Ussing chambers. The inhibition of GJIC resulted in a failure of PGE₂ to increase ASL volume in Calu-3 cells and in primary cultures of well-differentiated human airway epithelial cells. Thus, gap junctions coordinate a signaling network comprising CFTR, ADO-Rs, PARs, and EP-Rs, and are required for ASL volume homeostasis.
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Registered trials
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