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The ΔF508 Mutation Causes CFTR Misprocessing and Cystic Fibrosis–Like Disease in Pigs
Journal article   Peer reviewed

The ΔF508 Mutation Causes CFTR Misprocessing and Cystic Fibrosis–Like Disease in Pigs

Lynda S Ostedgaard, David K Meyerholz, Jeng-Haur Chen, Alejandro A Pezzulo, Philip H Karp, Tatiana Rokhlina, Sarah E Ernst, Robert A Hanfland, Leah R Reznikov, Paula S Ludwig, …
Science translational medicine, Vol.3(74), pp.74ra24-74ra24
03/16/2011
DOI: 10.1126/scitranslmed.3001868
PMCID: PMC3119077
PMID: 21411740

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Abstract

Cystic fibrosis (CF) is an autosomal recessive disease caused by mutations in the gene encoding the cystic fibrosis transmembrane conductance regulator (CFTR) anion channel. The most common CF-associated mutation is Delta F508, which deletes a phenylalanine in position 508. In vitro studies indicate that the resultant protein, CFTR-Delta F508, is misprocessed, although the in vivo consequences of this mutation remain uncertain. To better understand the effects of the Delta F508 mutation in vivo, we produced CFTR Delta F508/Delta F508 pigs. Our biochemical, immunocytochemical, and electrophysiological data on CFTR-Delta F508 in newborn pigs paralleled in vitro predictions. They also indicated that CFTR Delta F508/Delta F508 airway epithelia retain a small residual CFTR conductance, with maximal stimulation producing similar to 6% of wild-type function. Cyclic adenosine 3',5'-monophosphate (cAMP) agonists were less potent at stimulating current in CFTR Delta F508/Delta F508 epithelia, suggesting that quantitative tests of maximal anion current may overestimate transport under physiological conditions. Despite residual CFTR function, four older CFTR Delta F508/Delta F508 pigs developed lung disease similar to human CF. These results suggest that this limited CFTR activity is insufficient to prevent lung or gastrointestinal disease in CF pigs. These data also suggest that studies of recombinant CFTR-Delta F508 misprocessing predict in vivo behavior, which validates its use in biochemical and drug discovery experiments. These findings help elucidate the molecular pathogenesis of the common CF mutation and will guide strategies for developing new therapeutics.

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