ArticleAmerican journal of physiology. Lung cellular and molecular physiology2008
Low expression of the beta-ENaC subunit impairs lung fluid clearance in the mouse.
Article in American journal of physiology. Lung cellular and molecular physiology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Neonatal Genetic Variation in Steroid Metabolism and Key Respiratory Function Genes and Perinatal Outcomes in Single and Multiple Courses of Corticosteroids.American journal of perinatology · 2015Trial
- Neutrophil extracellular traps mediate mInternational journal of biological sciences · 2022Article
- Ferulic acid ameliorates lipopolysaccharide-induced tracheal injury via cGMP/PKGII signaling pathway.Respiratory research · 2021Article
- Alcohol inhibits alveolar fluid clearance through the epithelial sodium channel via the A2 adenosine receptor in acute lung injury.Molecular medicine reports · 2021Article
- Tissue Factor-Enriched Neutrophil Extracellular Traps Promote Immunothrombosis and Disease Progression in Sepsis-Induced Lung Injury.Frontiers in cellular and infection microbiology · 2021Article
- Autologous transplantation of adipose-derived stromal cells combined with sevoflurane ameliorates acute lung injury induced by cecal ligation and puncture in rats.Scientific reports · 2020Article
- Epithelial NaFrontiers in physiology · 2020Article
- Insulin ameliorates pulmonary edema through the upregulation of epithelial sodium channel via the PI3K/SGK1 pathway in mice with lipopolysaccharide‑induced lung injury.Molecular medicine reports · 2019Article
- Oxymatrine attenuates lipopolysaccharide-induced acute lung injury by activating the epithelial sodium channel and suppressing the JNK signaling pathway.Experimental animals · 2018Article
- Intermittent Hypoxia Increases the Severity of Bleomycin-Induced Lung Injury in Mice.Oxidative medicine and cellular longevity · 2018Article
- The function and regulation of acid-sensing ion channels (ASICs) and the epithelial Na(+) channel (ENaC): IUPHAR Review 19.British journal of pharmacology · 2016Review
- Regulation of epithelial sodium channels in urokinase plasminogen activator deficiency.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Conditioned media from mesenchymal stromal cells restore sodium transport and preserve epithelial permeability in an in vitro model of acute alveolar injury.American journal of physiology. Lung cellular and molecular physiology · 2014Article
- Autologous transplantation of adipose-derived stromal cells ameliorates ventilator-induced lung injury in rats.Journal of translational medicine · 2013Article
- Phosphatidylinositol phosphate-dependent regulation of Xenopus ENaC by MARCKS protein.American journal of physiology. Renal physiology · 2012Article
- Regulation of ENaC-mediated alveolar fluid clearance by insulin via PI3K/Akt pathway in LPS-induced acute lung injury.Respiratory research · 2012Article
- Nasal potential difference to detect Na+ channel dysfunction in acute lung injury.American journal of physiology. Lung cellular and molecular physiology · 2011Review
- Amiloride-sensitive sodium channels and pulmonary edema.Pulmonary medicine · 2011Article
- Incomplete reprogramming after fusion of human multipotent stromal cells and bronchial epithelial cells.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2010Article
- Rac1-mediated NADPH oxidase release of O2- regulates epithelial sodium channel activity in the alveolar epithelium.American journal of physiology. Lung cellular and molecular physiology · 2010Article
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9 authors at 1 institution in 1 country.
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No grant is acknowledged in the PubMed record.
Abstract
Transepithelial alveolar sodium (Na+) transport mediated by the amiloride-sensitive epithelial sodium channel (ENaC) constitutes the driving force for removal of fluid from the alveolar space. To define the role of the beta-ENaC subunit in vivo in the mature lung, we studied a previously established mouse strain harboring a disruption of the beta-ENaC gene locus resulting in low levels of beta-ENaC mRNA expression. Real-time RT-PCR experiments confirmed that beta-ENaC mRNA levels were decreased by >90% in alveolar epithelial cells from homozygous mutant (m/m) mice. beta-ENaC protein was undetected in lung homogenates from m/m mice by Western blotting, but alpha- and gamma-ENaC proteins were increased by 83% and 45%, respectively, compared with wild-type (WT) mice. At baseline, Na+-driven alveolar fluid clearance (AFC) was significantly reduced by 32% in m/m mice. Amiloride at the concentration 1 mM inhibited AFC by 75% and 34% in WT and m/m mice, respectively, whereas a higher concentration (5 mM) induced a 75% inhibition of AFC in both groups. The beta2-agonist terbutaline significantly increased AFC in WT but not in m/m mice. These results show that despite the compensatory increase in alpha- and gamma-ENaC protein expression observed in mutant mouse lung, low expression of beta-ENaC results in a moderate impairment of baseline AFC and in decreased AFC sensitivity to amiloride, suggesting a possible change in the stoichiometry of ENaC channels. Finally, adequate beta-ENaC expression appears to be required for AFC stimulation by beta2-agonists.
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