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1 Biomed Sci, University of Missouri-Columbia, Columbia, Missouri, United States; Veterinary Pathobiology, University of Missouri-Columbia, Columbia, Missouri, United States
2 Medicine, Medical Univ of S Carolina, Charleston, South Carolina, United States
3 Molecular Genetics, Biochem and Microbiology, U Cincinnati Col Med, Cincinnati, Ohio, United States
4 Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri, United States
5 Medicine, University of Cincinnati, Cincinnati, Ohio, United States
6 Biomed Sci, University of Missouri-Columbia, Columbia, Missouri, United States; Dalton Cardiovascular Research Center, University of Missouri-Columbia, Columbia, Missouri, United States
* To whom correspondence should be addressed. E-mail: clarkel{at}missouri.edu.
Basal HCO3- secretion across the duodenum has been shown in several species to principally involve the activity of apical membrane Cl-/HCO3- exchanger(s). To investigate the identity of relevant anion exchanger(s), studies were performed using wild-type (WT) mice and mice with gene-targeted deletion of Cl-/HCO3- exchangers localized to the apical membrane of murine duodenal villi: Slc26a3 (down-regulated in adenoma, DRA); Slc26a6 (putative anion transporter-1, PAT-1); and Slc4a9 (anion exchanger 4, AE4). RT-PCR of isolated villous epithelium demonstrated PAT-1, DRA, and AE4 mRNA expression. Using the pH-sensitive dye BCECF, anion exchange rates were measured across the apical membrane of epithelial cells in the upper villus of intact duodenal mucosa. Under basal conditions, Cl-/HCO3- exchange activity was reduced by 65-80% in PAT-1 (-), 30-40% in the DRA (-), and <5% in the AE4 (-) duodena as compared to WT. SO42-/HCO3- exchange was eliminated in the PAT-1 (-) but not affected in the DRA (-) and AE4 (-) duodena relative to WT. Intracellular pH (pHi) was reduced in the PAT-1(-) villous epithelium but increased to WT levels in the absence of CO2/HCO3- or during methazolamide treatment. Further studies under physiological conditions indicated active pHi compensation in the PAT-1(-) villous epithelium by conbined activities of the Na+/H+ exchanger NHE1 and Cl--dependent transport processes at the basolateral membrane. We conclude that 1) PAT-1 is the major contributor to basal Cl-/HCO3- and SO42-/HCO3- exchange across the apical membrane and 2) PAT-1 plays a role in pHi regulation in the upper villous epithelium of murine duodenum.
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