ArticleAmerican journal of physiology. Lung cellular and molecular physiology2012
Transgenic hCFTR expression fails to correct β-ENaC mouse lung disease.
Article in American journal of physiology. Lung cellular and molecular physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 16 citations in OpenAlex.
- The role of CFTR in spermatogenesis and sperm quality.Nature reviews. Urology · 2026Review
- Secretory Cells Dominate Airway CFTR Expression and Function in Human Airway Superficial Epithelia.American journal of respiratory and critical care medicine · 2021Article
- Is the ENaC Dysregulation in CF an Effect of Protein-Lipid Interaction in the Membranes?International journal of molecular sciences · 2021Review
- Role of CFTR in epithelial physiology.Cellular and molecular life sciences : CMLS · 2017Review
- Diffusion-sensitive optical coherence tomography for real-time monitoring of mucus thinning treatments.Proceedings of SPIE--the International Society for Optical Engineering · 2016Article
- CFTR and lung homeostasis.American journal of physiology. Lung cellular and molecular physiology · 2014Review
- Cigarette smoke and CFTR: implications in the pathogenesis of COPD.American journal of physiology. Lung cellular and molecular physiology · 2013Review
- Does epithelial sodium channel hyperactivity contribute to cystic fibrosis lung disease?The Journal of physiology · 2013Review
- Loss of Cftr function exacerbates the phenotype of Na(+) hyperabsorption in murine airways.American journal of physiology. Lung cellular and molecular physiology · 2013Article
- Status of fluid and electrolyte absorption in cystic fibrosis.Cold Spring Harbor perspectives in medicine · 2013Article
- The CFTR and ENaC debate: how important is ENaC in CF lung disease?American journal of physiology. Lung cellular and molecular physiology · 2012Article
- CFTR regulates early pathogenesis of chronic obstructive lung disease in βENaC-overexpressing mice.PloS one · 2012Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
The relationships between airway epithelial Cl(-) secretion-Na(+) absorption balance, airway surface liquid (ASL) homeostasis, and lung disease were investigated in selected transgenic mice. 1) To determine if transgenic overexpression of wild-type (WT) human CFTR (hCFTR) accelerated Cl(-) secretion and regulated Na(+) absorption in murine airways, we utilized a Clara cell secretory protein (CCSP)-specific promoter to generate mice expressing airway-specific hCFTR. Ussing chamber studies revealed significantly (∼2.5-fold) elevated basal Cl(-) secretory currents in CCSP-hCFTR transgenic mouse airways. Endogenous murine airway Na(+) absorption was not regulated by hCFTR, and these mice exhibited no lung disease. 2) We tested whether hCFTR, transgenically expressed on a transgenic mouse background overexpressing the β-subunit of the epithelial Na(+) channel (β-ENaC), restored ion transport balance and ASL volume homeostasis and ameliorated lung disease. Both transgenes were active in CCSP-hCFTR/β-ENaC transgenic mouse airways, which exhibited an elevated basal Cl(-) secretion and Na(+) hyperabsorption. However, the airway disease characteristic of β-ENaC mice persisted. Confocal studies of ASL volume homeostasis in cultured tracheal cells revealed ASL autoregulation to a height of ∼6 μm in WT and CCSP-hCFTR cultures, whereas ASL was reduced to <4 μm in β-ENaC and CCSP-hCFTR/β-ENaC cultures. We conclude that 1) hCFTR overexpression increases basal Cl(-) secretion but does not regulate Na(+) transport in WT mice and 2) transgenic hCFTR produces increased Cl(-) secretion, but not regulation of Na(+) channels, in β-ENaC mouse airways and does not ameliorate β-ENaC mouse 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.