Multiple calcium sources are required for intracellular calcium mobilization during gastric organoid epithelial repair.

Physiological Reports
Kristen A EngevikMarshall H Montrose

Abstract

Calcium (Ca2+ ) is a known accelerator for gastric wound repair. We have demonstrated in vivo and in vitro that intracellular Ca2+ increases in the gastric epithelial cells directly adjacent to a damaged cell, and that this Ca2+ rise is essential for the cellular migration that rapidly repairs the epithelium (restitution). While intracellular Ca2+ has been shown to be an important signaling factor during epithelial restitution, the source from which this intracellular Ca2+ originates remains unclear. Using gastric organoids derived from mice transgenic for a genetically encoded Ca2+ indicator, we sought to investigate the potential sources of intracellular Ca2+ mobilization. During confocal imaging, photodamage (PD) was induced to 1-2 gastric organoid epithelial cells and epithelial restitution measured simultaneously with changes in intracellular Ca2+ (measured as FRET/CFP ratio in migrating cells adjacent to the damaged area). Inhibition of voltage-gated Ca2+ channels (verapamil, 10 µM) or store-operated calcium entry (YM58483, 20 µM) resulted in delayed repair and dampened intracellular Ca2+ response. Furthermore, inhibition of phospholipase C (U73122, 10 µM) or inositol trisphosphate receptor (2-APB, 50 µM) likewise resulte...Continue Reading

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Citations

Jul 2, 2020·American Journal of Physiology. Lung Cellular and Molecular Physiology·Josephine C AdamsIrving H Zucker
Sep 10, 2020·Frontiers in Physiology·Richard BallwegTongli Zhang
May 21, 2021·Frontiers in Pharmacology·Yan ChangZui Pan
Sep 4, 2021·Current Opinion in Gastroenterology·Susan J Hagen

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Methods Mentioned

BETA
transgenic
simple light
PCR

Software Mentioned

Metamorph
Image J

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