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白三烯B4和血小板活化因子刺激下多形核白细胞中肌动蛋白聚合/解聚的快速振荡

Rapid oscillations of actin polymerization/depolymerization in polymorphonuclear leukocytes stimulated by leukotriene B4 and platelet-activating factor.

作者信息

Omann G M, Rengan R, Hoffman J F, Linderman J J

机构信息

Veterans Administration Medical Center, Ann Arbor, MI 48105, USA.

出版信息

J Immunol. 1995 Dec 1;155(11):5375-81.

PMID:7594553
Abstract

We previously showed that activation of polymorphonuclear leukocytes by leukotriene B4 (LTB4) and platelet-activating factor produces a rapidly oscillating actin polymerization/depolymerization response. In this study, we show that 1) oscillations are not due to the stimulated cyclic release of autocoids that could bind to cell surface receptors and activate subsequent cycles; 2) oscillations are not related to oscillations of ligand binding; and 3) the particular kinetic pattern is a property of the receptor, not of the binding constants of the ligand. The major conclusion of these studies is that the oscillations are a property of the intrinsic signaling pathways triggered by these chemoattractants. We also questioned whether increased actin nucleation activity was induced by LTB4 and found that, although LTB4 induced a transient actin nucleation response, there was not a direct correlation between oscillations of the actin polymerization/depolymerization and the actin nucleation activity. This suggests that processes other than actin nucleation, such as release of monomeric actin from monomer sequestering proteins and regulation of depolymerization, are likely to be involved.

摘要

我们之前表明,白三烯B4(LTB4)和血小板活化因子激活多形核白细胞会产生快速振荡的肌动蛋白聚合/解聚反应。在本研究中,我们表明:1)振荡并非由于自分泌物质的刺激循环释放,这些自分泌物质可与细胞表面受体结合并激活后续循环;2)振荡与配体结合的振荡无关;3)特定的动力学模式是受体的特性,而非配体结合常数的特性。这些研究的主要结论是,振荡是由这些趋化因子触发的内在信号通路的特性。我们还质疑LTB4是否诱导了肌动蛋白成核活性增加,结果发现,尽管LTB4诱导了短暂的肌动蛋白成核反应,但肌动蛋白聚合/解聚的振荡与肌动蛋白成核活性之间没有直接关联。这表明,除肌动蛋白成核外的其他过程,如单体肌动蛋白从单体隔离蛋白的释放和解聚调节,可能也参与其中。

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