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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Neutrophil microtubules suppress polarity and enhance directional migration
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Neutrophil microtubules suppress polarity and enhance directional migration

机译：中性粒细胞微管抑制极性并增强方向迁移

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How do microtubules, which maintain and direct polarity of many eukaryotic cells, regulate polarity of blood neutrophils? In sharp contrast to most cells, disrupting a neutrophil's microtubule network with nocodazole causes it to polarize and migrate [Niggli, V. (2003) J. Cell Sci. 116, 813-822]. Nocodazole induces the same responses in differentiated HL-60 cells, a model neutrophil cell line, and reduces their chemotactic prowess by causing them to pursue abnormally circuitous paths in migrating toward a stationary point source of an attractant, f-Met-Leu-Phe (fMLP). The chemotactic defect stems from dramatic nocodazole-induced imbalance between the divergent, opposed fMLP-induced "backness" and "frontness" signals responsible for neutrophil polarity. Nocodazole (ⅰ) stimulates backness by increasing Rho- and actomyosin-dependent contractility, as reported by Niggli, and also (ⅱ) impairs fMLP-dependent frontness: pseudopods are flatter, contain less F-actin, and show decreased membrane translocation of PH-Akt-GFP, a fluorescent marker for 3′-phosphoinositide lipids. Inhibiting backness with a pharmacologic inhibitor of a Rho-dependent kinase substantially reverses nocodazole's effects on chemotaxis, straightness of migration paths, morphology, and PH-Akt-GFP translocation. Thus, microtubules normally balance backness vs. frontness signals, preventing backness from reducing the strength of pseudopods and from impairing directional migration.
机译：维持并指导许多真核细胞极性的微管如何调节血液中性粒细胞的极性？与大多数细胞形成鲜明对比的是，用诺考达唑破坏嗜中性白细胞的微管网络会使其极化并迁移[Niggli，V.（2003）J. Cell Sci。Acad.Sci.USA，88：3879-1877。 116，813-822]。 Nocodazole在分化的HL-60细胞（一种模型嗜中性粒细胞系）中诱导相同的反应，并通过使它们沿着异常的circuit回路径迁移到引诱剂f-Met-Leu-Phe的固定点源上来降低其趋化能力（ fMLP）。趋化性缺陷源于诺考达唑诱导的发散的，相反的fMLP诱导的“嗜中性粒细胞极性”信号的“反面”和“正面”信号之间的显着失衡。如Niggli报道的那样，诺考达唑（by）通过增加Rho-和肌动球蛋白依赖性的收缩力来刺激后背，并且（ⅱ）损害fMLP依赖性的前沿性：假足更平坦，F-肌动蛋白含量降低，PH-的膜移位降低Akt-GFP，3'-磷酸肌醇脂质的荧光标记。用Rho依赖性激酶的药理学抑制剂抑制背痛实质上可以逆转诺考达唑对趋化性，迁移路径的直度，形态和PH-Akt-GFP易位的影响。因此，微管通常会平衡反面信号与正面信号之间的距离，从而防止反面信号降低伪足的强度并削弱定向迁移。

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