Muller William A
Northwestern University Feinberg School of Medicine, 303 E Chicago Ave, Ward Building 3-140, Chicago, IL 60611, USA.
Circ Res. 2009 Jul 31;105(3):223-30. doi: 10.1161/CIRCRESAHA.109.200717.
A great deal of progress has been made recently in understanding the molecules and mechanisms that regulate transendothelial migration of leukocytes, or diapedesis, a critical step in the inflammatory response. This review focuses mainly on the active role of the endothelial cell in this process as it occurs at endothelial cell borders. It discusses some of the many molecules that have been reported to play a role in transendothelial migration and asks why so many molecules seem to be involved. The concept is emerging that diapedesis itself can be dissected into sequential steps controlled by specific molecule(s) at the endothelial cell border. Several mechanisms have been shown to play a critical role in transendothelial migration including signals derived from clustering of apically disposed intercellular adhesion molecule-1 and vascular cell adhesion molecule-1, disruption or loosening of adherens junctions, and targeted recycling of platelet/endothelial cell adhesion molecule and other molecules from the recently described lateral border recycling compartment. A hypothesis that integrates the various known mechanisms is proposed.
最近在理解调节白细胞跨内皮迁移（即白细胞渗出，炎症反应中的关键步骤）的分子和机制方面取得了很大进展。本综述主要关注内皮细胞在此过程中在内皮细胞边界处的积极作用。它讨论了许多据报道在跨内皮迁移中起作用的分子，并探讨了为何似乎有如此多的分子参与其中。一种新的概念正在形成，即白细胞渗出本身可被分解为由内皮细胞边界处特定分子控制的连续步骤。已经证明几种机制在跨内皮迁移中起关键作用，包括顶端排列的细胞间粘附分子-1和血管细胞粘附分子-1聚集产生的信号、黏附连接的破坏或松弛，以及血小板/内皮细胞粘附分子和其他分子从最近描述的侧向边界回收区室的靶向回收。本文提出了一个整合各种已知机制的假说。
