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Department of Physiology, Dartmouth Medical School, Hanover, New Hampshire 03755
Sodium butyrate and its derivatives are useful therapeutic
agents for the treatment of genetic diseases including urea cycle disorders, sickle cell disease, thalassemias, and possibly cystic fibrosis (CF). Butyrate partially restores cAMP-activated
Cl
secretion in CF
epithelial cells by stimulating 
F508 cystic fibrosis transmembrane
conductance regulator (F508-CFTR) gene expression and increasing the
amount of F508-CFTR in the plasma membrane. Because the effect of
butyrate on Cl secretion by
renal epithelial cells has not been reported, we examined the effects
of chronic butyrate treatment (15-18 h) on the function,
expression, and localization of CFTR fused to the green fluorescent
protein (GFP-CFTR) in stably transfected MDCK cells. We report that
sodium butyrate reduced Cl
secretion across MDCK cells, yet increased apical membrane GFP-CFTR expression 25-fold and increased apical membrane
Cl currents 30-fold.
Although butyrate also increased Na-K-ATPase protein expression
twofold, the drug reduced the activity of the Na-K-ATPase by 55%. Our
findings suggest that butyrate inhibits cAMP-stimulated
Cl secretion across MDCK
cells in part by reducing the activity of the Na-K-ATPase.
green fluorescent protein; cystic fibrosis; gene expression; cystic fibrosis transmembrane conductance regulator; adenosine 3',5'-cyclic monophosphate
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