PDF(Pubmed)
Abstract：
Within the bloodstream, monocytes must traverse the microvasculature to prevent leukostasis, which is the entrapment of monocytes within the confines of the microvasculature. Using the model cell line, THP-1, and VCAM-1 coated channels to simulate the microvasculature surface, we demonstrate that monocytes predominantly adopt an amoeboid phenotype, which is characterized by the formation of blebs. As opposed to cortical actin flow in leader blebs, cell movement is correlated with myosin contraction at the cell rear. It was previously documented that cofilin-1 promotes cortical actin turnover at leader bleb necks in melanoma cells. In monocytes, our data suggest that cofilin-1 promotes the local upregulation of myosin contractility through actin cytoskeleton remodeling. In support of this concept, cofilin-1 is found to localize to a single cell edge. Moreover, the widespread upregulation of myosin contractility was found to inhibit migration. Thus, monocytes within the microvasculature may avoid entrapment by adopting an amoeboid mode of migration.
摘要：
在血液中，单核细胞必须穿过微脉管系统以防止白细胞淤积，这是单核细胞在微脉管系统范围内的截留。使用模型细胞系，THP-1和VCAM-1包被通道，以模拟微脉管系统表面，我们证明单核细胞主要采用变形虫表型，其特征是形成气泡。与前导气泡中的皮质肌动蛋白流相反，细胞运动与细胞后部的肌球蛋白收缩有关。先前有文献记载，cofilin-1可促进黑素瘤细胞前导囊颈处的皮质肌动蛋白更新。在单核细胞中，我们的数据表明，cofilin-1通过肌动蛋白细胞骨架重塑促进肌球蛋白收缩性的局部上调。为了支持这一概念，cofilin-1被发现定位到单个细胞边缘。此外，发现肌球蛋白收缩性的广泛上调抑制了迁移。因此，微脉管系统中的单核细胞可以通过采用变形虫迁移模式来避免截留。
