TY - JOUR
T1 - Wound-induced calcium waves in alveolar type II cells
AU - Hinman, E. Lee
AU - Beilman, Greg J.
AU - Groehler, Kristine E.
AU - Sammak, Paul J.
PY - 1997
Y1 - 1997
N2 - 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.
AB - 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.
KW - Acute lung injury
KW - Alveolar epithelial cells
KW - Intercellular signaling
KW - Intracellular calcium stores
KW - Mechanical injury
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U2 - 10.1152/ajplung.1997.273.6.l1242
DO - 10.1152/ajplung.1997.273.6.l1242
M3 - Article
C2 - 9435580
AN - SCOPUS:0031416790
SN - 1040-0605
VL - 273
SP - L1242-L1248
JO - American Journal of Physiology - Lung Cellular and Molecular Physiology
JF - American Journal of Physiology - Lung Cellular and Molecular Physiology
IS - 6 17-6
ER -