Deletion of the chloride transporter Slc26a7 causes distal renal tubular acidosis and impairs gastric acid secretion

Jie Xu, Penghong Song, Suguru Nakamura, Marian Miller, Sharon Barone, Seth L. Alper, Brigitte Riederer, Janina Bonhagen, Lois J. Arend, Hassane Amlal, Ursula Seidler, Manoocher Soleimani

Research output: Contribution to journalArticle

Abstract

SLC26A7 (human)/Slc26a7 (mouse) is a recently identified chloride-base exchanger and/or chloride transporter that is expressed on the basolateral membrane of acid-secreting cells in the renal outer medullary collecting duct (OMCD) and in gastric parietal cells. Here, we show that mice with genetic deletion of Slc26a7 expression develop distal renal tubular acidosis, as manifested by metabolic acidosis and alkaline urine pH. In the kidney, basolateral Cl-/HCO3- exchange activity in acid-secreting intercalated cells in the OMCD was significantly decreased in hypertonic medium (a normal milieu for the medulla) but was reduced only mildly in isotonic medium. Changing from a hypertonic to isotonic medium (relative hypotonicity) decreased the membrane abundance of Slc26a7 in kidney cells in vivo and in vitro. In the stomach, stimulated acid secretion was significantly impaired in isolated gastric mucosa and in the intact organ. We propose that SLC26A7 dysfunction should be investigated as a potential cause of unexplained distal renal tubular acidosis or decreased gastric acid secretion in humans.

Original languageEnglish (US)
Pages (from-to)29470-29479
Number of pages10
JournalJournal of Biological Chemistry
Volume284
Issue number43
DOIs
StatePublished - Oct 23 2009

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Cell Biology

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    Xu, J., Song, P., Nakamura, S., Miller, M., Barone, S., Alper, S. L., Riederer, B., Bonhagen, J., Arend, L. J., Amlal, H., Seidler, U., & Soleimani, M. (2009). Deletion of the chloride transporter Slc26a7 causes distal renal tubular acidosis and impairs gastric acid secretion. Journal of Biological Chemistry, 284(43), 29470-29479. https://doi.org/10.1074/jbc.M109.044396