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Wound-induced calcium waves in alveolar type II cells

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 Ca concentration ([Ca ] ) began at the edge of the wound and propa...

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Bibliographic Details
Published in:American journal of physiology. Lung cellular and molecular physiology 1997-12, Vol.273 (6), p.L1242
Main Authors: Hinman, Lee E, Beilman, Greg J, Groehler, Kristine E, Sammak, Paul J
Format: Article
Language:English
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Summary: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 Ca concentration ([Ca ] ) began at the edge of the wound and propagated outward as a wave for at least 300 μm. The [Ca ] wave was due to both influx of extracellular Ca and release of intracellular Ca stores. Reducing Ca influx with brief treatments of ethylene glycol-bis(β-aminoethyl ether)- N, N, N', N'-tetraacetic acid or Gd reduced both the amplitude and the apparent speed. Draining intracellular Ca stores by pretreatment with cyclopiazonic acid eliminated the [Ca ] wave. Therefore, the [Ca ] wave depended critically on intracellular Ca stores. [Ca ] elevations propagated over a break in the monolayer, suggesting that extracellular pathways were involved. Furthermore, extracellular factors from injured cells elevated [Ca ] in uninjured cultures. We conclude that wounding produces a [Ca ] wave in surviving cells and part of this response is mediated by soluble factors released into the extracellular space during injury.
ISSN:1522-1504