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首页> 外文期刊>Cell motility and the cytoskeleton >Periodic formation of nascent lamellae is driven by changes in the stable F-actin pool of polymorphonuclear neutrophils after stimulation with chemotactic peptide and cross-linking of CD18 or CD61.
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Periodic formation of nascent lamellae is driven by changes in the stable F-actin pool of polymorphonuclear neutrophils after stimulation with chemotactic peptide and cross-linking of CD18 or CD61.

机译：趋化肽刺激和CD18或CD61交联后，多形核中性粒细胞的稳定F-肌动蛋白池发生变化，从而驱动新生薄片的周期性形成。

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Cell motility and changes in cell shape are largely powered by actin polymerization and depolymerization. Eight to ten second periodic changes in human polymorphonuclear neutrophil (PMN) shape were detected by video-image analysis of PMN crawling on a surface and by right angle light scattering (RALS) in suspended PMN. However, sustained RALS oscillations in suspended PMN requires pre-treatment with an inhibitor of phosphatidylinositol 3-kinase or an activator of protein kinase C. Here, we show that cross-linking of the beta(2) (CD18) or beta(3) (CD61), but not beta(1) (CD 29) integrins in the presence of a low dose of formyl-Methionyl-Leucyl-Phenylalanine (fMLP) enables similar 8-s periodic RALS oscillations in suspended PMN in response to stimulation with two consecutive doses of chemoattractants. This effect did not appear to be due to increased surface expression of CD18 or CD61. RALS oscillations occurred in phase with 8-s oscillations in the stable F-actin pool and peaks in F-actin correlated with predominance of cells exhibiting a nascent lamella. Thus, simulation of surface attachment by CD18 and CD61 cross-linking after exposure to fMLP in suspended cells supports shape oscillations that are the result of actin-driven cyclic extension/retraction of nascent lamellae at the same frequency as the shape changes previously observed in crawling PMN. Copyright 1999 Wiley-Liss, Inc.
机译：肌动蛋白的聚合和解聚作用在很大程度上促进了细胞运动和细胞形状的变化。通过对表面上爬行的PMN进行视频图像分析并通过悬浮PMN中的直角光散射（RALS）检测到人类多形核中性粒细胞（PMN）形状的八到十秒的周期性变化。但是，在悬浮的PMN中持续的RALS振荡需要用磷脂酰肌醇3-激酶抑制剂或蛋白激酶C的活化剂进行预处理。在这里，我们显示出beta（2）（CD18）或beta（3）的交联（CD61）而不是beta（1）（CD 29）整合素，在低剂量的甲酰基-甲硫基-亮氨酰-苯丙氨酸（fMLP）存在的情况下，响应于两次刺激，悬浮PMN中的类似的8-s周期性RALS振荡连续剂量的趋化剂。这种作用似乎不是由于CD18或CD61的表面表达增加所致。 RALS振荡与稳定的F-肌动蛋白池中的8-s振荡同相发生，并且F-肌动蛋白的峰值与表现出新生薄片的细胞优势相关。因此，在悬浮细胞中暴露于fMLP后通过CD18和CD61交联进行表面附着的模拟可支持形状振荡，这是肌动蛋白驱动的新生薄片周期性扩展/收缩的频率，与先前在爬行过程中观察到的形状变化频率相同PMN。版权所有1999 Wiley-Liss，Inc.

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