Reduction of SNAP25 in acid secretion defect of Foxl1-|-gastric parietal cells
Reduction of SNAP25 in acid secretion defect of Foxl1-|-gastric parietal cells
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DOI：
10.1016/j.bbrc.2004.05.209
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发表时间：
2004-07-30
影响因子：
3.1
通讯作者：
Ohno, H
中科院分区：
文献类型：
--
作者：
Kato, Y;Fukamachi, H;Ohno, H
Foxl1 是一种在胃肠道间充质中表达的翼状螺旋转录因子。在缺乏 Foxl1 的情况下，壁细胞无法响应包括 cAMP 在内的各种促分泌剂刺激而分泌胃酸。尽管 Foxl1 缺陷小鼠中仍然存在大量壁细胞，但观察到 H+、K+、ATPase 表达显着下降。超微结构分析表明，Foxl1缺陷小鼠的胃酸分泌缺陷主要是由于细胞质管泡结构与心尖小管质膜融合受损所致。在参与膜融合事件的分子中，只有 SNAP25 的 mRNA 表达显着下降，这可能导致 Foxl1 缺陷小鼠壁细胞酸分泌受损，而 H+,K+ -ATPase 表达的减少有助于产生额外的效果。 (C) 2004 Elsevier Inc. 保留所有权利。
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. (C) 2004 Elsevier Inc. All rights reserved.