Document Detail

Bile-acid-induced calcium signaling in mouse esophageal epithelial cells.
MedLine Citation:
PMID:  22005467     Owner:  NLM     Status:  Publisher    
In patients with gastroesophageal reflux disease (GERD), esophageal exposure to both acid and duodenogastroesophageal reflux are more common than to acid reflux alone, suggesting that acidic bile acid in duodenal juice may contribute to the pathophysiology and severity of GERD. However, the mechanism whereby esophageal mucosal epithelial cells react to bile acid remains unclear. We visually examined the real-time response of mouse esophageal epithelial cells to bile acids using calcium (Ca(2+))-imaging methods. We investigated the effects of seven different bile acids. After stimulation for a few minutes, only Deoxycholate (DCA) under acidic conditions caused a elevation of intracellular Ca(2+) concentration ([Ca(2+)](i))in the cells in dose- and pH-dependent manners. Conjugated bile acids had no effect on the cells. Viability assay of the cells in the presence of DCA was in good agreement with the calcium imaging data. Besides, DCA-induced [Ca(2+)](i) increase in acidic conditions was observed not only in isolated primary cultured cells, but also in cells in the stratified squamous epithelium. This study suggests that DCA can pass through the anatomical barrier of the esophageal epithelium and induce calcium signaling in epithelial cells in a pH-dependent manner. This supports the hypothesis that bile acid reflux together with gastric acid can affect the esophageal mucosa, even under reflux times of a few minutes.
Takahiro Yamada; Yusuke Ishida; Yukiko Nakamura; Shoichi Shimada
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2011-10-7
Journal Detail:
Title:  Biochemical and biophysical research communications     Volume:  -     ISSN:  1090-2104     ISO Abbreviation:  -     Publication Date:  2011 Oct 
Date Detail:
Created Date:  2011-10-18     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0372516     Medline TA:  Biochem Biophys Res Commun     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2011. Published by Elsevier Inc.
Department of Neuroscience and Cell Biology, Osaka University Graduate School of Medicine, Osaka, Japan.
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