Microtubule asymmetry during neutrophil polarization and migration
Microtubule asymmetry during neutrophil polarization and migration
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DOI：
10.1091/mbc.e02-04-0241
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发表时间：
2002-12-01
影响因子：
3.3
通讯作者：
Maxfield, FR
中科院分区：
文献类型：
--
作者：
Eddy, RJ;Pierini, LM;Maxfield, FR
人类多形核中性粒细胞（PMNs）在化学引诱剂刺激下的细胞极性发展，其特征是由圆形形态迅速转变为极化形态，其前部为片足，后部为尾足。在PMN极化过程中，微管（MT）阵列经历了一个戏剧性的向尾足的重新定向，在运动期间维持，不需要大规模的MT分解或细胞粘附到基质上。在极化和运动期间，MT被排除在领先的片层之外，但是用肌球蛋白轻链激酶抑制剂（ML-7）或肌动蛋白破坏药物细胞松弛素D治疗会导致MT阵列的扩大和MT进入板足。MT阵列在刺激前解聚导致10%的细胞通过延长两个相反的侧板足而失去极性。这些多极细胞显示出板层特异性标记talin和尾足类特异性标记CD44的定位改变。综上所述，这些结果表明，f -肌动蛋白和肌球蛋白ii依赖力导致MT不对称的发展和维持，这可能在PMN迁移过程中增强细胞极性。
The development of cell polarity in response to chemoattractant stimulation in human polymorphonuclear neutrophils, (PMNs) is characterized by the rapid conversion from round to polarized morphology with a leading lamellipod at the front and a uropod at the rear. During PMN polarization, the microtubule (MT) array undergoes a dramatic reorientation toward the uropod that is maintained during motility and does not require large-scale MT disassembly or cell adhesion to the substratum MTs are excluded from the leading lamella during polarization and motility, but treatment with a myosin light chain kinase inhibitor (ML-7) or the actin-disrupting drug cytochalasin D causes an expansion of the MT array and penetration of MTs into the lamellipod. Depolymerization of the MT array before stimulation caused 10% of the cells to lose their polarity by extending two opposing lateral lamellipodia. These multipolar cells showed altered localization of a leading lamella-specific marker, talin, and a uropod-specific marker, CD44. In summary, these results indicate that F-actin- and myosin II-dependent forces lead to the development and maintenance of MT asymmetry that may act to reinforce cell polarity during PMN migration.