Reduction of SNAP25 in acid secretion defect of Foxl1-/- gastric parietal cells

Biochemical and Biophysical Research Communications
Yasutaka KatoHiroshi Ohno

Abstract

Foxl1 is a winged helix transcription factor expressed in the mesenchyme of the gastrointestinal tract. In the absence of Foxl1, parietal cells fail to secrete gastric acid in response to various secretagogue stimuli including cAMP. A marked decrease in H+,K(+)-ATPase expression was observed even though a substantial number of parietal cells still existed in Foxl1-deficient mice. Ultrastructural analysis suggested that the gastric acid secretion defect in Foxl1-deficient mice is mainly due to impairment in the fusion of cytoplasmic tubulovesicular structures to the apical canalicular plasma membrane. Among the molecules involved in the membrane fusion event, only SNAP25 showed a significant decrease in mRNA expression, which likely caused the impairment in acid secretion from parietal cells in Foxl1-deficient mice, with the reduction in H+,K(+)-ATPase expression contributing to additional effect.

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Citations

Oct 13, 2005·Current Opinion in Gastroenterology·Mitchell L Schubert
Feb 13, 2010·Annual Review of Physiology·John G Forte, Lixin Zhu
Sep 14, 2016·Developmental Biology·Caitlin D Hanlon, Deborah J Andrew
Jul 31, 2007·Genesis : the Journal of Genetics and Development·Sara D SackettKlaus H Kaestner
Feb 14, 2006·American Journal of Physiology. Gastrointestinal and Liver Physiology·Masumi Takano-MaruyamaHiroshi Ohno

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