KCNQ1 loss-of-function mutation impairs gastric acid secretion in mice.
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.
Pan
Qin
Q
Department of Cardiology, Tongji Hospital, Tongji University School of Medicine, Shanghai, China.
Ma
Jun
J
Zhou
Qinshu
Q
Li
Jun
J
Tang
Yongqing
Y
Liu
Yi
Y
Yang
Yiqing
Y
Xiao
Junjie
J
Peng
Luying
L
Li
Pengjuan
P
Liang
Dandan
D
Zhang
Hong
H
Chen
Yi-Han
YH
D000704:Analysis of Variance; D000818:Animals; D005744:Gastric Acid / Q000378:metabolism*; D017506:H(+)-K(+)-Exchanging ATPase / Q000378:metabolism; D006863:Hydrogen-Ion Concentration; D051657:KCNQ1 Potassium Channel / Q000235:genetics* / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D009154:Mutation / Q000235:genetics; D010295:Parietal Cells, Gastric / Q000378:metabolism*
D051657:KCNQ1 Potassium Channel; C496910:Kcnq1 protein, mouse; D017506:H(+)-K(+)-Exchanging ATPase