1. Reduction of SNAP25 in acid secretion defect of Foxl1-/- gastric parietal cells.
- Author
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Kato Y, Fukamachi H, Takano-Maruyama M, Aoe T, Murahashi Y, Horie S, Suzuki Y, Saito Y, Koseki H, and Ohno H
- Subjects
- Animals, Bethanechol pharmacology, Bucladesine pharmacology, Cells, Cultured, Forkhead Transcription Factors, Mice, Parietal Cells, Gastric drug effects, Pentagastrin pharmacology, Sodium-Potassium-Exchanging ATPase metabolism, Synaptosomal-Associated Protein 25, DNA-Binding Proteins deficiency, Gastric Acid metabolism, Membrane Proteins metabolism, Nerve Tissue Proteins metabolism, Parietal Cells, Gastric cytology, Parietal Cells, Gastric metabolism, Transcription Factors deficiency
- 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. more...
- Published
- 2004
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