ArticleAmerican journal of physiology. Lung cellular and molecular physiology2011
Regulation of endogenous ENaC functional expression by CFTR and ΔF508-CFTR in airway epithelial cells.
Article in American journal of physiology. Lung cellular and molecular physiology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 65 citations in OpenAlex.
- ENaC is a host susceptibility factor to bacterial infections in cystic fibrosis context.Communications biology · 2025Article
- Sex differences in airway disease: estrogen and airway surface liquid dynamics.Biology of sex differences · 2024Review
- Recommended Tool Compounds for Modifying the Cystic Fibrosis Transmembrane Conductance Regulator Channel Variants.ACS pharmacology & translational science · 2024Review
- Review
- Q1291H-CFTR molecular dynamics simulations andFrontiers in molecular biosciences · 2023Article
- Loss of CFTR function is associated with reduced bitter taste receptor-stimulated nitric oxide innate immune responses in nasal epithelial cells and macrophages.Frontiers in immunology · 2023Article
- Prevalence and Mechanisms of Mucus Accumulation in COVID-19 Lung Disease.American journal of respiratory and critical care medicine · 2022Article
- Downregulation of epithelial sodium channel (ENaC) activity in cystic fibrosis cells by epigenetic targeting.Cellular and molecular life sciences : CMLS · 2022Article
- Association of cystic fibrosis transmembrane conductance regulator with epithelial sodium channel subunits carrying Liddle's syndrome mutations.American journal of physiology. Lung cellular and molecular physiology · 2021Article
- DNA Methylation Patterns Correlate with the Expression ofInternational journal of molecular sciences · 2021Article
- Downregulation of epithelial sodium channel (ENaC) activity in human airway epithelia after low temperature incubation.BMJ open respiratory research · 2021Article
- Capsaicin-Loaded Chitosan Nanocapsules for wtCFTR-mRNA Delivery to a Cystic Fibrosis Cell Line.Biomedicines · 2020Article
- Chitosan Nanocomplexes for the Delivery of ENaC Antisense Oligonucleotides to Airway Epithelial Cells.Biomolecules · 2020Article
- SPLUNC1 degradation by the cystic fibrosis mucosal environment drives airway surface liquid dehydration.The European respiratory journal · 2018Article
- Cystic fibrosis transmembrane conductance regulator modulators: precision medicine in cystic fibrosis.Current opinion in pediatrics · 2018Review
- Inhibition of NKCC1 Modulates Alveolar Fluid Clearance and Inflammation in Ischemia-Reperfusion Lung Injury via TRAF6-Mediated Pathways.Frontiers in immunology · 2018Article
- Mathematical model reveals role of nucleotide signaling in airway surface liquid homeostasis and its dysregulation in cystic fibrosis.Proceedings of the National Academy of Sciences of the United States of America · 2017Article
- Signaling Cascade Involved in Rapid Stimulation of Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) by Dexamethasone.International journal of molecular sciences · 2017Article
- Effects ofAmerican journal of physiology. Cell physiology · 2017Review
- Differentiation of human bronchial epithelial cells: role of hydrocortisone in development of ion transport pathways involved in mucociliary clearance.American journal of physiology. Cell physiology · 2016Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
The functional expression of the epithelial sodium channel (ENaC) appears elevated in cystic fibrosis (CF) airway epithelia, but the mechanism by which this occurs is not clear. We tested the hypothesis that the cystic fibrosis transmembrane conductance regulator (CFTR) alters the trafficking of endogenously expressed human ENaC in the CFBE41o⁻ model of CF bronchial epithelia. Functional expression of ENaC, as defined by amiloride-inhibited short-circuit current (I(sc)) in Ussing chambers, was absent under control conditions but present in CFBE41o⁻ parental and ΔF508-CFTR-overexpressing cells after treatment with 1 μM dexamethasone (Dex) for 24 h. The effect of Dex was mimicked by incubation with the glucocorticoid hydrocortisone but not with the mineralocorticoid aldosterone. Application of trypsin to the apical surface to activate uncleaved, "near-silent" ENaC caused an additional increase in amiloride-sensitive I(sc) in the Dex-treated cells and was without effect in the control cells, suggesting that Dex increased ENaC cell surface expression. In contrast, Dex treatment did not stimulate amiloride-sensitive I(sc) in CFBE41o⁻ cells that stably express wild-type (wt) CFTR. CFBE41o⁻ wt cells also had reduced expression of α- and γ-ENaC compared with parental and ΔF508-CFTR-overexpressing cells. Furthermore, application of trypsin to the apical surface of Dex-treated CFBE41o⁻ wt cells did not stimulate amiloride-sensitive I(sc), suggesting that ENaC remained absent from the surface of these cells even after Dex treatment. We also tested the effect of trafficking-corrected ΔF508-CFTR on ENaC functional expression. Incubation with 1 mM 4-phenylbutyrate synergistically increased Dex-induced ENaC functional expression in ΔF508-CFTR-overexpressing cells. These data support the hypothesis that wt CFTR can regulate the whole cell, functional, and surface expression of endogenous ENaC in airway epithelial cells and that absence of this regulation may foster ENaC hyperactivity in CF airway epithelia.
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