Abstract：
:It has been a few decades since Ca(2+) was identified as one of the important factors that can accelerate gastric wound repair as well as contribute to epithelial homeostasis and regulation of gastric secretions. The mechanistic basis has remained largely unexplored in vivo because it was not possible to track in real time either intracellular Ca(2+) mobilization or wound repair in living tissues. Recent advances in technology, such as combining high resolution light microscopy and genetically encoded Ca(2+) reporters in mice, now allow the monitoring of Ca(2+) mobilization during gastric epithelial cell restitution. Ca(2+) is a ubiquitous second messenger that influences numerous cellular processes, including gastric acid/bicarbonate secretion, mucus secretion, and cell migration. We have demonstrated that cytosolic Ca(2+) mobilization within the restituting gastric epithelial cells is a central signal driving small wound repair. However, extracellular Ca(2+) is also mobilized in the juxtamucosal luminal space above a wound, and evidence suggests extracellular Ca(2+) is a third messenger that also promotes gastric epithelial restitution. Interplay between intracellular and extracellular Ca(2+) is necessary for efficient gastric epithelial restitution.
journal_name
Curr Opin Pharmacoljournal_title
Current opinion in pharmacologyauthors
Aihara E,Montrose MHdoi
10.1016/j.coph.2014.07.012subject
Has Abstractpub_date
2014-12-01 00:00:00pages
76-83eissn
1471-4892issn
1471-4973pii
S1471-4892(14)00087-3journal_volume
19pub_type
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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journal_title：Current opinion in pharmacology
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