Transendothelial migration (TEM) of leukocytes is the step in leukocyte emigration in which the leukocyte actually leaves the blood vessel to carry out its role in the inflammatory response. It is therefore, arguably the most critical step in emigration. This review focuses on two of the many aspects of this process that have seen important recent developments. The adhesion molecules, PECAM (CD31) and CD99 that regulate two major steps in TEM, do so by regulating specific signals. PECAM initiates the signaling pathway responsible for the calcium flux that is required for TEM. Calcium enters through the cation channel TRPC6 and recruits the first wave of trafficking of membrane from the lateral border recycling compartment (LBRC). CD99 signals through soluble adenylate cyclase to activate protein kinase A to recruit a second wave of LBRC trafficking. Another process that is critical for TEM is transient removal of VE-cadherin from the site of TEM. However, the local signaling pathways that are responsible for this appear to be different from those that open the junctions to increase vascular permeability.

中文翻译：

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调节跨内皮迁移的局部信号。

白细胞的跨内皮迁移（TEM）是白细胞迁移的步骤，在该步骤中，白细胞实际上离开了血管，在炎症反应中发挥作用。因此，可以说这是移民中最关键的一步。这篇综述着重于这一过程的许多方面中的两个方面，这些方面已经看到了重要的近期发展。调节TEM中两个主要步骤的粘附分子PECAM（CD31）和CD99通过调节特定信号来实现。PECAM启动负责TEM所需钙通量的信号传导途径。钙通过阳离子通道TRPC6进入，并从侧边界回收室（LBRC）吸收了第一批膜运输。CD99通过可溶性腺苷酸环化酶发出信号以激活蛋白激酶A，以募集第二批LBRC运输。对TEM至关重要的另一个过程是从TEM部位瞬时去除VE-钙粘蛋白。但是，造成这种情况的局部信号传导途径似乎不同于那些打开接头以增加血管通透性的途径。