ArticlePloS one2012
CFTR regulates early pathogenesis of chronic obstructive lung disease in βENaC-overexpressing mice.
Article in PloS one, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.
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Who cites it
34 citing papers in PubMed, 55 citations in OpenAlex.
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- SLPI deficiency alters airway protease activity and induces cell recruitment in a model of muco-obstructive lung disease.Frontiers in immunology · 2024Article
- Inhalation of nicotine-containing electronic cigarette vapor exacerbates the features of COPD by inducing ferroptosis in βENaC-overexpressing mice.Frontiers in immunology · 2024Article
- Biologically Relevant Murine Models of ChronicPathogens (Basel, Switzerland) · 2023Article
- A novel thiol-saccharide mucolytic for the treatment of muco-obstructive lung diseases.The European respiratory journal · 2023Article
- Cystic fibrosis transmembrane conductance regulator in COPD: a role in respiratory epithelium and beyond.The European respiratory journal · 2023Review
- Genetic Deletion ofInternational journal of molecular sciences · 2022Article
- Congenital Deletion ofInternational journal of molecular sciences · 2021Article
- Electronic Cigarette Exposure Enhances Lung Inflammatory and Fibrotic Responses in COPD Mice.Frontiers in pharmacology · 2021Article
- Therapeutic Inhibition of Cathepsin S Reduces Inflammation and Mucus Plugging in AdultMediators of inflammation · 2021Article
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- 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
- CFTR mutation enhances Dishevelled degradation and results in impairment of Wnt-dependent hematopoiesis.Cell death & disease · 2018Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundFactors determining the onset and severity of chronic obstructive pulmonary disease remain poorly understood. Previous studies demonstrated that airway surface dehydration in βENaC-overexpressing (βENaC-Tg) mice on a mixed genetic background caused either neonatal mortality or chronic obstructive lung disease suggesting that the onset of lung disease was modulated by the genetic background.
methodsTo test this hypothesis, we backcrossed βENaC-Tg mice onto two inbred strains (C57BL/6 and BALB/c) and studied effects of the genetic background on neonatal mortality, airway ion transport and airway morphology. Further, we crossed βENaC-Tg mice with CFTR-deficient mice to validate the role of CFTR in early lung disease.
resultsWe demonstrate that the C57BL/6 background conferred increased CFTR-mediated Cl(-) secretion, which was associated with decreased mucus plugging and mortality in neonatal βENaC-Tg C57BL/6 compared to βENaC-Tg BALB/c mice. Conversely, genetic deletion of CFTR increased early mucus obstruction and mortality in βENaC-Tg mice.
conclusionsWe conclude that a decrease or absence of CFTR function in airway epithelia aggravates the severity of early airway mucus obstruction and related mortality in βENaC-Tg mice. These results suggest that genetic or environmental factors that reduce CFTR activity may contribute to the onset and severity of chronic obstructive pulmonary disease and that CFTR may serve as a novel therapeutic target.
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