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内皮细胞连接处的细胞黏附动力学:血管内皮钙黏蛋白是主要参与者。

Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player.

作者信息

Vestweber Dietmar, Winderlich Mark, Cagna Giuseppe, Nottebaum Astrid F

机构信息

Max-Planck-Institute of Molecular Biomedicine, Röntgenstrasse 20, Münster, Germany.

出版信息

Trends Cell Biol. 2009 Jan;19(1):8-15. doi: 10.1016/j.tcb.2008.10.001. Epub 2008 Nov 17.

DOI:10.1016/j.tcb.2008.10.001
PMID:19010680
Abstract

The regulation of endothelial cell contacts is of central importance for the barrier function of the blood vessel wall and for the control of leukocyte extravasation. In addition, the plasticity of endothelial cell contacts is regulated during angiogenesis by growth factors, such as vascular endothelial growth factor and angiopoietin-1. Despite the participation of several adhesion molecules and receptors in the control of endothelial cell contacts, most of the currently known mechanisms involve vascular endothelial cadherin (VE-cadherin), an essential adhesion molecule for the stability of endothelial junctions. Here, we focus on recent results showing how leukocytes and angiogenic factors regulate endothelial junctions.

摘要

内皮细胞接触的调节对于血管壁的屏障功能以及白细胞外渗的控制至关重要。此外,在血管生成过程中,内皮细胞接触的可塑性受到生长因子的调节,如血管内皮生长因子和血管生成素-1。尽管有几种粘附分子和受体参与了内皮细胞接触的控制,但目前已知的大多数机制都涉及血管内皮钙粘蛋白(VE-钙粘蛋白),这是一种对内皮连接稳定性至关重要的粘附分子。在这里,我们重点关注最近的研究结果,这些结果显示了白细胞和血管生成因子如何调节内皮连接。

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Cell adhesion dynamics at endothelial junctions: VE-cadherin as a major player.内皮细胞连接处的细胞黏附动力学:血管内皮钙黏蛋白是主要参与者。
Trends Cell Biol. 2009 Jan;19(1):8-15. doi: 10.1016/j.tcb.2008.10.001. Epub 2008 Nov 17.
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Breaking the VE-cadherin bonds.破坏血管内皮钙黏蛋白键。
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Jumping the barrier: VE-cadherin, VEGF and other angiogenic modifiers in cancer.跨越障碍:血管内皮钙黏蛋白、血管内皮生长因子和其他血管生成调节剂在癌症中的作用。
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