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.
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Acknowledgments
This work was supported by the National Science Fund for Distinguished Young Scholars (30425016), the National Science Fund of China (30330290, 30528011 and 30470961), the “973” Program Fund of China (2007CB512100), the “863” Program Fund of China (2007AA02Z438), the Program Fund for Outstanding Medical Academic Leader of Shanghai, China, the Program Fund for Shanghai Subject Chief Scientist, China, the Yangtze Scholars Program Fund by the Ministry of Education, China, and the Program Fund for Innovative Research Team by the Ministry of Education, China (all to Yi-Han Chen).
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The authors Q. Pan, J. Ma, Q. Zhou, J. Li, and Y. Tang contributed equally to this work.
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Pan, Q., Ma, J., Zhou, Q. et al. KCNQ1 loss-of-function mutation impairs gastric acid secretion in mice. Mol Biol Rep 37, 1329–1333 (2010). https://doi.org/10.1007/s11033-009-9511-9
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DOI: https://doi.org/10.1007/s11033-009-9511-9