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• W2148309013 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." @default.
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• W2148309013 date "2012-01-15" @default.
• W2148309013 modified "2023-09-27" @default.
• W2148309013 title "Transgenic hCFTR expression fails to correct β-ENaC mouse lung disease" @default.
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• W2148309013 doi "https://doi.org/10.1152/ajplung.00083.2011" @default.
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