Meshulam T, Proto P, Diamond R D, Melnick D A
J Immunol. 1986 Sep 15;137(6):1954-60.
Stimulation of neutrophils by chemoattractants is followed by a rapid, transient rise in cytosolic calcium concentration. The role of calcium in activation of cell movement and related responses was examined by selectively chelating extracellular or both extra- and intracellular calcium. Removal of calcium from the extracellular medium did not alter the cytosolic calcium concentration (Quin 2 fluorescence, 110 to 120 nM) of unstimulated neutrophils and did not dramatically affect the rise induced by formyl peptide. Despite the intact Quin 2 response, depletion of extracellular calcium partially inhibited chemotaxis, adherence to substrate, and polarization (increased forward light scatter) in response to formyl peptide. Loading neutrophils with Quin 2 in the absence of calcium depressed cytosolic Ca2+ to 10 to 20 nM and abrogated a detectable rise with formyl peptide stimulation. Depletion of intracellular calcium further inhibited chemotaxis and polarization, although neutrophils still demonstrated significant directed migration and shape change to formyl peptide (30 to 40% of control) without an increase in Quin 2 fluorescence. Other neutrophil responses related to chemotaxis (decreased right-angle light scatter, actin polymerization) were minimally affected by depletion of calcium from either site. The data indicate that neutrophil chemotaxis and related responses to formyl peptide may be activated by intracellular signals not detectable with Quin 2.
趋化因子刺激中性粒细胞后，胞质钙浓度会迅速短暂升高。通过选择性螯合细胞外钙或细胞外和细胞内钙，研究了钙在细胞运动激活及相关反应中的作用。从细胞外培养基中去除钙，未改变未受刺激的中性粒细胞的胞质钙浓度（喹啉2荧光，110至120 nM），也未显著影响甲酰肽诱导的钙浓度升高。尽管喹啉2反应完好，但细胞外钙耗竭部分抑制了对甲酰肽的趋化性、对底物的黏附以及极化（前向光散射增加）。在无钙情况下用喹啉2加载中性粒细胞，可使胞质Ca2+降至10至20 nM，并消除甲酰肽刺激后可检测到的钙浓度升高。细胞内钙耗竭进一步抑制趋化性和极化，尽管中性粒细胞在无喹啉2荧光增加的情况下，对甲酰肽仍表现出显著的定向迁移和形态变化（为对照的30%至40%）。其他与趋化性相关的中性粒细胞反应（直角光散射减少、肌动蛋白聚合）受任何一个部位钙耗竭的影响最小。数据表明，中性粒细胞趋化性及对甲酰肽的相关反应可能由喹啉2无法检测到的细胞内信号激活。
