Wound-induced calcium waves in alveolar type II cells
Wound-induced calcium waves in alveolar type II cells
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DOI：
10.1152/ajplung.1997.273.6.l1242
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发表时间：
1997-12-01
影响因子：
4.9
通讯作者：
Sammak, PJ
中科院分区：
文献类型：
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作者：
Hinman, LE;Beilman, GJ;Sammak, PJ
肺泡II型上皮细胞（ATII）在急性肺损伤后重新填充肺泡。我们假设伤害会在附近的幸存者中发出信号。当大鼠ATII单层细胞受伤时，细胞内游离Ca ~（2+）浓度（[Ca ~（2+）]（i））从伤口边缘开始升高，并以波的形式向外传播至少300 μ m。[Ca ~（2+）]（i）波是由于细胞外Ca ~（2+）内流和细胞内Ca ~（2+）库释放所致。用乙二醇-双（β-氨乙基醚）-N，N，N '，N'-四乙酸或Gd ~（3+）短暂处理，减少Ca ~（2+）内流，既降低幅度，又降低表观速度。用环匹阿尼酸预处理细胞内Ca ~（2+）库使[Ca ~（2+）]（i）波消失。因此，[Ca ~（2+）]（i）波主要依赖于细胞内的Ca ~（2+）库。[Ca2+]（i）升高在单层破裂处传播，表明涉及细胞外途径。此外，来自受损细胞的细胞外因子在未受损的培养物中升高[Ca 2 +]（i）。我们的结论是，创伤产生的[Ca 2 +]（i）波在存活的细胞和这种反应的一部分是由可溶性因子释放到细胞外空间在损伤过程中介导的。
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 mu m. 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(beta-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.