ArticleThe Journal of biological chemistry2010
Airway surface liquid volume regulation determines different airway phenotypes in liddle compared with betaENaC-overexpressing mice.
Article in The Journal of biological chemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
46 citing papers in PubMed, 76 citations in OpenAlex.
- Reflection confocal microscopy for quantitative assessment of airway surface layer dysregulation and pharmacological rescue in cystic fibrosis under near-physiological conditions.Scientific reports · 2025Article
- Structural insights into subunit-dependent functional regulation in epithelial sodium channels.Structure (London, England : 1993) · 2025Article
- Repetitive ozone exposure worsens features of muco-inflammatory disease in developedFrontiers in toxicology · 2025Article
- Dynamic measurement of airway surface liquid volume with anLab on a chip · 2024Article
- Epithelial NaComprehensive Physiology · 2024Review
- SCNN1B regulates the proliferation, migration, and collagen deposition of human lung fibroblasts.In vitro cellular & developmental biology. Animal · 2023Article
- 30-Min Exposure to Tobacco Smoke Influences Airway Ion Transport-An In Vitro Study.Current oncology (Toronto, Ont.) · 2023Article
- Article
- Role of epithelial sodium channel-related inflammation in human diseases.Frontiers in immunology · 2023Review
- Genetic Deletion ofInternational journal of molecular sciences · 2022Article
- Age-Related Differences in Structure and Function of Nasal Epithelial Cultures From Healthy Children and Elderly People.Frontiers in immunology · 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
- Linking Fibrotic Remodeling and Ultrastructural Alterations of Alveolar Epithelial Cells after Deletion ofInternational journal of molecular sciences · 2021Article
- Congenital Deletion ofInternational journal of molecular sciences · 2021Article
- Therapeutic Inhibition of Cathepsin S Reduces Inflammation and Mucus Plugging in AdultMediators of inflammation · 2021Article
- ENaC inhibition in cystic fibrosis: potential role in the new era of CFTR modulator therapies.The European respiratory journal · 2020Review
- Paraoxonase 3 functions as a chaperone to decrease functional expression of the epithelial sodium channel.The Journal of biological chemistry · 2020Article
- Expression and function of Anoctamin 1/TMEM16A calcium-activated chloride channels in airways of in vivo mouse models for cystic fibrosis research.Pflugers Archiv : European journal of physiology · 2018Article
- Rebuttal from Stephen M. Stick and André Schultz.The Journal of physiology · 2018Article
- Lung disease phenotypes caused by overexpression of combinations of α-, β-, and γ-subunits of the epithelial sodium channel in mouse airways.American journal of physiology. Lung cellular and molecular physiology · 2018Article
Corrections and comments
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Authors and funding
14 authors at 4 institutions in 3 countries.
Funding
Abstract
Studies in cystic fibrosis patients and mice overexpressing the epithelial Na(+) channel beta-subunit (betaENaC-Tg) suggest that raised airway Na(+) transport and airway surface liquid (ASL) depletion are central to the pathogenesis of cystic fibrosis lung disease. However, patients or mice with Liddle gain-of-function betaENaC mutations exhibit hypertension but no lung disease. To investigate this apparent paradox, we compared the airway phenotype (nasal versus tracheal) of Liddle with CFTR-null, betaENaC-Tg, and double mutant mice. In mouse nasal epithelium, the region that functionally mimics human airways, high levels of CFTR expression inhibited Liddle epithelial Nat channel (ENaC) hyperfunction. Conversely, in mouse trachea, low levels of CFTR failed to suppress Liddle ENaC hyperfunction. Indeed, Na(+) transport measured in Ussing chambers ("flooded" conditions) was raised in both Liddle and betaENaC-Tg mice. Because enhanced Na(+) transport did not correlate with lung disease in these mutant mice, measurements in tracheal cultures under physiologic "thin film" conditions and in vivo were performed. Regulation of ASL volume and ENaC-mediated Na(+) absorption were intact in Liddle but defective in betaENaC-Tg mice. We conclude that the capacity to regulate Na(+) transport and ASL volume, not absolute Na(+) transport rates in Ussing chambers, is the key physiologic function protecting airways from dehydration-induced lung disease.
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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.