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1 Medicine, University of Cincinnati, Cincinnati, OH, USA
* To whom correspondence should be addressed. E-mail: Manoocher.Soleimani{at}uc.edu.
Bicarbonate secretion by gastric mucous cells is essential for protection against acid injury and peptic ulcer. Here we report the identification of an apical bicarbonate transporter in gastric surface epithelial cells. Northern hybridization and RT-PCR demonstrate the expression of this transporter, also known as SLC26A9, in mouse and rat stomach and trachea (but not kidney). In situ hybridization in mouse stomach showed abundant expression of SLC26A9 in surface epithelial cells with apical localization on immunofluorescence labeling. Functional studies in HEK 293 cells demonstrated that SLC26A9 mediates Cl-/HCO3- exchange and is also capable of transporting Cl-independent bicarbonate extrusion. Unlike other anion exchangers or transport proteins reported to date, SLC26A9 activity is inhibited by NH4+. The inhibitory effect of NH4+ on gastric bicarbonate secretion was also indicated by a reduced gastric juxtamucousal pH in rat stomach in vivo. This is the first report on the inhibition of bicarbonate transport in vitro and the reduction in juxtamucosal pH in stomach in vivo by NH4+. Given its critical localization on apical membrane of surface epithelial cells, its ability to transport bicarbonate and inhibition by NH4+ we propose that SLC26A9 mediates bicarbonate secretion in surface epithelial cells and is essential for protection against acid injury in the stomach. Disease states that are associated with increased NH3/NH4+ generation (such as H. Pylori) may impair gastric bicarbonate secretion and therefore predispose to peptic ulcer by inhibiting SLC26A9.
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