Leukocyte transendothelial migration (TEM) takes place across micron-wide gaps in specific post-capillary venules generated by the transmigrating leukocyte. Because endothelial cells contain a dense cytoskeletal network, transmigrating leukocytes must overcome these mechanical barriers as they squeeze their nuclei through endothelial gaps and pores. Recent findings suggest that endothelial cells are not a passive barrier, and upon engagement by transmigrating leukocytes trigger extensive dynamic modifications of their actin cytoskeleton. Unexpectedly, endothelial contractility functions as a restrictor of endothelial gap enlargement rather than as a facilitator of gap formation as was previously suggested. In this review we discuss current knowledge regarding how accurately timed endothelial actin-remodeling events are triggered by squeezing leukocytes and coordinate leukocyte TEM while preserving blood vessel integrity.

中文翻译：

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内皮屏障的白细胞破坏：肌动蛋白链接。

白细胞跨内皮迁移（TEM）发生在由迁移的白细胞产生的特定毛细血管后小静脉中的微米级间隙中。由于内皮细胞包含密集的细胞骨架网络，因此迁移的白细胞在通过内皮间隙和孔挤压细胞核时必须克服这些机械障碍。最近的发现表明内皮细胞不是被动屏障，并且在通过迁移的白细胞参与时触发其肌动蛋白细胞骨架的广泛动态修饰。出乎意料的是，内皮收缩性起着限制内皮间隙增大的作用，而不是像以前所建议的那样促进间隙形成。