KCNQ1 loss-of-function mutation impairs gastric acid secretion in mice

Mol Biol Rep. 2010 Mar;37(3):1329-33. doi: 10.1007/s11033-009-9511-9. Epub 2009 Mar 21.

Abstract

The KCNQ1 channel is abundantly expressed in the gastric parietal cells. Although the functional coupling of KCNQ1 with the H(+)/K(+)-ATPase has already been confirmed on the basis of pharmacological kinetics, the effect of a KCNQ1 loss-of-function mutation on gastric acidification remains unclear. In this study, parietal cells and gastric glands from both C57BL/6 J mice (normal control) and J343 mice (mice with a KCNQ1 loss-of-function mutation) were isolated to study the effects of KCNQ1 on gastric acidification. We found that the mutation limited intracellular acidification of parietal cells and H(+) secretion of the stomach in response to histamine. Thus, a KCNQ1 loss-of-function mutation may impair gastric acid secretion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Analysis of Variance
  • Animals
  • Gastric Acid / metabolism*
  • H(+)-K(+)-Exchanging ATPase / metabolism
  • Hydrogen-Ion Concentration
  • KCNQ1 Potassium Channel / genetics*
  • KCNQ1 Potassium Channel / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Mutation / genetics
  • Parietal Cells, Gastric / metabolism*

Substances

  • KCNQ1 Potassium Channel
  • Kcnq1 protein, mouse
  • H(+)-K(+)-Exchanging ATPase