Wound-induced calcium waves in alveolar type II cells

E. Lee Hinman, Greg J. Beilman, Kristine E. Groehler, Paul J. Sammak

Research output: Contribution to journalArticle

38 Scopus citations

Abstract

Alveolar type II epithelial (ATII) cells repopulate the alveolus after acute lung injury. We hypothesized that injury would initiate signals in nearby survivors. When rat ATII monolayers were wounded, elevations in intracellular free Ca2+ concentration ([Ca2+](i)) began at the edge of the wound and propagated outward as a wave for at least 300 μm. The [Ca2+](i) wave was due to both influx of extracellular Ca2+ and release of intracellular Ca2+ stores. Reducing Ca2+ influx with brief treatments of ethylene glycol-bis(β-aminoethyl ether)-N,N,N',N'-tetraacetic acid or Gd3+ reduced both the amplitude and the apparent speed. Draining intracellular Ca2+ stores by pretreatment with cyclopiazonic acid eliminated the [Ca2+](i) wave. Therefore, the [Ca2+](i) wave depended critically on intracellular Ca2+ stores. [Ca2+](i) elevations propagated over a break in the monolayer, suggesting that extracellular pathways were involved. Furthermore, extracellular factors from injured cells elevated [Ca2+](i) in uninjured cultures. We conclude that wounding produces a [Ca2+](i) wave in surviving cells and part of this response is mediated by soluble factors released into the extracellular space during injury.

Original languageEnglish (US)
Pages (from-to)L1242-L1248
JournalAmerican Journal of Physiology - Lung Cellular and Molecular Physiology
Volume273
Issue number6 17-6
DOIs
StatePublished - 1997

Keywords

  • Acute lung injury
  • Alveolar epithelial cells
  • Intercellular signaling
  • Intracellular calcium stores
  • Mechanical injury

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