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首页> 外文期刊>Cell motility and the cytoskeleton >Induction of cortical oscillations in spreading cells by depolymerization of microtubules.
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Induction of cortical oscillations in spreading cells by depolymerization of microtubules.

机译：通过微管解聚诱导扩散细胞中的皮质振荡。

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Actomyosin-based cortical contractility is a common feature of eukaryotic cells but the capability to produce rhythmic contractions is found in only a few types such as cardiomyocytes. Mechanisms responsible for the acquisition of this capability remain largely unknown. Rhythmic contractility can be induced in non-muscle cells by microtubule depolymerization. Spreading epithelial cells and fibroblasts in which microtubules were depolymerized with nocodazole or colcemid underwent rhythmic oscillations of the body that lasted for several hours before the cells acquired a stable, flattened shape. By contrast, control cells spread and flattened into discoid shapes in a smooth and regular manner. Quantitative analysis of the oscillations showed that they have a period of about 50 seconds. The kinase inhibitors, HA 1077 and H7, and the more specific rho-kinase inhibitor, Y 27632, caused the oscillations to immediately cease and the cells to become flat. Transient increases in cytoplasmic calcium preceded the contractile phase of the oscillations. Wrinkle formation by cells plated on elastic substrata indicated that the contractility of colcemid-treated cells increased in comparison to controls but was drastically decreased after HA 1077 addition. These data suggest that an intact microtubular system normally prevents pulsations by moderating excessive rho-mediated actin myosin contractility. Possible mechanistic interactions between rho-mediated and calcium activated contractile pathways that could produce morphological oscillations are discussed. Copyright 2001 Wiley-Liss, Inc.
机译：基于肌动蛋白的皮质收缩力是真核细胞的共同特征，但仅在几种类型的细胞（如心肌细胞）中发现产生节律性收缩的能力。负责获得此功能的机制在很大程度上仍然未知。通过微管解聚可以在非肌肉细胞中诱导节律性收缩力。散布的上皮细胞和成纤维细胞（其中微管与诺考达唑或秋水仙碱解聚）经历了有节奏的身体振荡，持续了数小时，之后细胞才获得稳定，扁平的形状。相比之下，对照细胞以平滑且规则的方式散布成扁平状。振荡的定量分析表明，振荡的周期约为50秒。激酶抑制剂HA 1077和H7，以及更具体的rho激酶抑制剂Y 27632，导致振荡立即停止并且细胞变得扁平。细胞质钙的瞬时增加先于振荡的收缩期。接种在弹性基质上的细胞产生的皱纹表明，与对照相比，用秋水仙素处理的细胞的收缩力增加，但在添加HA 1077后急剧下降。这些数据表明，完整的微管系统通常可通过调节过度的rh介导的肌动蛋白肌球蛋白收缩力来防止搏动。讨论了可能介导形态振荡的rho介导的和钙激活的收缩途径之间可能的机制相互作用。版权所有2001 Wiley-Liss，Inc.

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