ArticlePloS one2017
Impaired PGE2-stimulated Cl- and HCO3- secretion contributes to cystic fibrosis airway disease.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 12 citations in OpenAlex.
- Assessing the consistency of iPSC and animal models in cystic fibrosis modelling: A meta-analysis.PloS one · 2022Pooled it
- Therapeutic potential of synergistic mucociliary clearance for cystic fibrosis airways by β-adrenergic plus cholinergic agonists.The Journal of clinical investigation · 2026Article
- Redox Imbalance in Cystic Fibrosis: The Multifaceted Role of Oxidative Stress.Pharmaceuticals (Basel, Switzerland) · 2025Review
- Regulating arachidonic acid metabolism: a novel strategy to prevent colorectal inflammatory cancer transformation.Journal of Cancer · 2025Review
- Mucus-targeting therapies of defective mucus clearance for cystic fibrosis: A short review.Current opinion in pharmacology · 2022Review
- Receptor-mediated activation of CFTR via prostaglandin signaling pathways in the airway.American journal of physiology. Lung cellular and molecular physiology · 2022Article
- The protective effect of the EP2 receptor on TGF-β1 induced podocyte injury via the PI3K / Akt signaling pathway.PloS one · 2018Article
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAirway mucociliary clearance (MCC) is an important defense mechanism against pulmonary infections and is compromised in cystic fibrosis (CF). Cl- and HCO3- epithelial transport are integral to MCC. During pulmonary infections prostaglandin E2 (PGE2) production is abundant.
aimTo determine the effect of PGE2 on airway Cl- and HCO3- secretion and MCC in normal and CF airways.
methodsWe examined PGE2 stimulated MCC, Cl- and HCO3- secretion using ferret trachea, human bronchial epithelial cell cultures (CFBE41o- with wildtype CFTR (CFBE41 WT) or homozygous F508del CFTR (CFBE41 CF) and human normal bronchial submucosal gland cell line (Calu-3) in Ussing chambers with or without pH-stat.
resultsPGE2 stimulated MCC in a dose-dependent manner and was partially impaired by CFTRinh-172. PGE2-stimulated Cl- current in ferret trachea was partially inhibited by CFTRinh-172, with niflumic acid eliminating the residual current. CFBE41 WT cell monolayers produced a robust Cl- and HCO3- secretory response to PGE2, both of which were completely inhibited by CFTRinh-172. CFBE41 CF cells exhibited no response to PGE2. In Calu-3 cells, PGE2 stimulated Cl- and HCO3- secretion. Cl- secretion was partially inhibited by CFTRinh-172, with additional inhibition by niflumic acid. HCO3- secretion was completely inhibited by CFTRinh-172.
conclusionsPGE2 stimulates bronchotracheal MCC and this response is decreased in CF. In CF airway, PGE2-stimulated Cl- and HCO3- conductance is impaired and may contribute to decreased MCC. There remains a CFTR-independent Cl- current in submucosal glands, which if exploited, could represent a means of improving airway Cl- secretion and MCC in CF.
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