In vivo epithelial wound repair requires mobilization of endogenous intracellular and extracellular calcium

J Biol Chem. 2013 Nov 22;288(47):33585-33597. doi: 10.1074/jbc.M113.488098. Epub 2013 Oct 11.

Abstract

We report that a localized intracellular and extracellular Ca(2+) mobilization occurs at the site of microscopic epithelial damage in vivo and is required to mediate tissue repair. Intravital confocal/two-photon microscopy continuously imaged the surgically exposed stomach mucosa of anesthetized mice while photodamage of gastric epithelial surface cells created a microscopic lesion that healed within 15 min. Transgenic mice with an intracellular Ca(2+)-sensitive protein (yellow cameleon 3.0) report that intracellular Ca(2+) selectively increases in restituting gastric epithelial cells adjacent to the damaged cells. Pretreatment with U-73122, indomethacin, 2-aminoethoxydiphenylborane, or verapamil inhibits repair of the damage and also inhibits the intracellular Ca(2+) increase. Confocal imaging of Fura-Red dye in luminal superfusate shows a localized extracellular Ca(2+) increase at the gastric surface adjacent to the damage that temporally follows intracellular Ca(2+) mobilization. Indomethacin and verapamil also inhibit the luminal Ca(2+) increase. Intracellular Ca(2+) chelation (1,2-bis(o-aminophenoxy)ethane-N,N,N',N'-tetraacetic acid/acetoxymethyl ester, BAPTA/AM) fully inhibits intracellular and luminal Ca(2+) increases, whereas luminal calcium chelation (N-(2-hydroxyetheyl)-ethylendiamin-N,N,N'-triacetic acid trisodium, HEDTA) blocks the increase of luminal Ca(2+) and unevenly inhibits late-phase intracellular Ca(2+) mobilization. Both modes of Ca(2+) chelation slow gastric repair. In plasma membrane Ca-ATPase 1(+/-) mice, but not plasma membrane Ca-ATPase 4(-/-) mice, there is slowed epithelial repair and a diminished gastric surface Ca(2+) increase. We conclude that endogenous Ca(2+), mobilized by signaling pathways and transmembrane Ca(2+) transport, causes increased Ca(2+) levels at the epithelial damage site that are essential to gastric epithelial cell restitution in vivo.

Keywords: Calcium; Calcium Imaging; Calcium Signaling; Cell Migration; Fluorescence Resonance Energy Transfer (FRET); Fura Red; Photodamage; Two-photon Microscopy; Yellow Cameleon.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Anti-Inflammatory Agents, Non-Steroidal / pharmacology
  • Boron Compounds / pharmacology
  • Calcium / metabolism*
  • Calcium Channel Blockers / pharmacology
  • Calcium Signaling*
  • Calcium-Transporting ATPases / antagonists & inhibitors
  • Calcium-Transporting ATPases / genetics
  • Calcium-Transporting ATPases / metabolism
  • Chelating Agents / pharmacology
  • Edetic Acid / analogs & derivatives
  • Edetic Acid / pharmacology
  • Egtazic Acid / analogs & derivatives
  • Egtazic Acid / pharmacology
  • Estrenes / pharmacology
  • Gastric Mucosa / injuries*
  • Gastric Mucosa / metabolism
  • Gastric Mucosa / pathology
  • Indomethacin / pharmacology
  • Mice
  • Mice, Knockout
  • Phosphodiesterase Inhibitors / pharmacology
  • Pyrrolidinones / pharmacology
  • Verapamil / pharmacology
  • Wound Healing*

Substances

  • Anti-Inflammatory Agents, Non-Steroidal
  • Boron Compounds
  • Calcium Channel Blockers
  • Chelating Agents
  • Estrenes
  • Phosphodiesterase Inhibitors
  • Pyrrolidinones
  • 1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dione
  • 1,2-bis(2-aminophenoxy)ethane N,N,N',N'-tetraacetic acid acetoxymethyl ester
  • Egtazic Acid
  • Edetic Acid
  • Verapamil
  • 2-aminoethoxydiphenyl borate
  • Calcium-Transporting ATPases
  • N-(hydroxyethyl)ethylenediaminetriacetic acid
  • Calcium
  • Indomethacin