alexa Genetically determined heterogeneity of lung disease in a mouse model of airway mucus obstruction.
Toxicology

Toxicology

Journal of Drug Metabolism & Toxicology

Author(s): LivraghiButrico A, Grubb BR, Kelly EJ, Wilkinson KJ, Yang H, , LivraghiButrico A, Grubb BR, Kelly EJ, Wilkinson KJ, Yang H,

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Abstract Mucus clearance is an important airway innate defense mechanism. Airway-targeted overexpression of the epithelial Na(+) channel β-subunit [encoded by sodium channel nonvoltage gated 1, beta subunit (Scnn1b)] in mice [Scnn1b-transgenic (Tg) mice] increases transepithelial Na(+) absorption and dehydrates the airway surface, which produces key features of human obstructive lung diseases, including mucus obstruction, inflammation, and air-space enlargement. Because the first Scnn1b-Tg mice were generated on a mixed background, the impact of genetic background on disease phenotype in Scnn1b-Tg mice is unknown. To explore this issue, congenic Scnn1b-Tg mice strains were generated on C57BL/6N, C3H/HeN, BALB/cJ, and FVB/NJ backgrounds. All strains exhibited a two- to threefold increase in tracheal epithelial Na(+) absorption, and all developed airway mucus obstruction, inflammation, and air-space enlargement. However, there were striking differences in neonatal survival, ranging from 5 to 80\% (FVB/NJ This article was published in Physiol Genomics and referenced in Journal of Drug Metabolism & Toxicology

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