Randriamampita C, Trautmann A
Laboratoire de Neurobiologie, Ecole Normale Supérieure, Paris, France.
FEBS Lett. 1989 Jun 5;249(2):199-206. doi: 10.1016/0014-5793(89)80624-6.
In single mouse macrophages stimulated by platelet-activating factor (PAF), the intracellular calcium concentration (Cai) monitored with fura-2 at room temperature presents a biphasic increase, including a transient and a more sustained component. After pulse administration of PAF, the first phase lasts for a few seconds and reaches a peak value of 0.5-1 microM Ca2+ at high PAF concentration. The amplitude of this peak is independent of extracellular Ca2+ concentration, suggesting that the initial Ca2+ transient is due to the release of Ca2+ from intracellular stores. The second phase of the response lasts for several minutes; its maximum amplitude is reached 1-2 min after the brief initial PAF stimulation. This phase, suppressed in zero external Ca2+ and increased in 10 mM Ca2+, is probably due to influx of Ca2+ through the plasma membrane. This secondary Ca2+ increase is blocked by 10-50 microM lanthanum. At low PAF concentration, the initial Ca2+ transient is not followed by a second phase, showing that the initial rises of Ca2+ and of its activator (presumably inositol trisphosphate) are not sufficient to trigger the second phase of Ca2+ increase.
在由血小板活化因子(PAF)刺激的单个小鼠巨噬细胞中,在室温下用fura - 2监测的细胞内钙浓度(Cai)呈现双相增加,包括一个短暂的和一个更持久的成分。在脉冲给予PAF后,第一阶段持续几秒钟,在高PAF浓度下达到0.5 - 1 microM Ca2+的峰值。该峰值的幅度与细胞外Ca2+浓度无关,表明初始Ca2+瞬变是由于细胞内储存的Ca2+释放所致。反应的第二阶段持续几分钟;在短暂的初始PAF刺激后1 - 2分钟达到其最大幅度。该阶段在零细胞外Ca2+中受到抑制,在10 mM Ca2+中增加,可能是由于Ca2+通过质膜内流所致。这种继发性Ca2+增加被10 - 50 microM镧阻断。在低PAF浓度下,初始Ca2+瞬变之后没有第二阶段,表明Ca2+及其激活剂(可能是肌醇三磷酸)的初始升高不足以触发Ca2+增加的第二阶段。