Nitric oxide disrupts VE-cadherin complex in murine microvascular endothelial cells
Nitric oxide disrupts VE-cadherin complex in murine microvascular endothelial cells
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DOI：
10.1016/s0006-291x(03)00546-1
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发表时间：
2003-04-25
影响因子：
3.1
通讯作者：
Rojas, A
中科院分区：
文献类型：
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作者：
González, D;Herrera, B;Rojas, A
血管内皮钙粘蛋白（VE-cadherin）定位于粘附连接处，参与控制血管通透性。越来越多的证据表明，一氧化氮调节液体和蛋白质的运动出脉管系统。在本文中，我们研究了NO是否可以破坏ve -钙粘蛋白复合体。我们发现，通过免疫沉淀分析、细胞ELISA和Northern blot分析，两种NO供体（SIN-1和SNAP）治疗显著降低了小鼠微血管内皮细胞系（H5V）中VE-cadherin的含量。-和-连环蛋白也被发现受到两个NO供体的影响。此外，在体内和体外模型中，一氧化氮供体诱导的复合物破坏与血管通透性增加相关。这些结果清楚地表明NO在血管通透性中的作用。(C) 2003 Elsevier Science（美国）版权所有。
Vascular endothelial cadherin (VE-cadherin), which is localized at adherent junctions, is involved in the control of vascular permeability. A growing body of evidence indicates that NO modulates the movement of fluid and proteins out of the vasculature. In this paper, we investigated whether NO can disrupt the VE-cadherin complex. We found that treatment with two NO donors (SIN-1 and SNAP) markedly reduced the amount of VE-cadherin in a murine microvascular endothelial cell line (H5V) as demonstrated by immunoprecipitation analysis, cellular ELISA, and Northern blot analysis. beta- and gamma-Catenins were also found to be affected by the two NO donors. Moreover, the disruption of the complex, induced by NO donors, correlated with increases in vascular permeability using both in vivo and in vitro models. These results clearly demonstrate a role for NO in vascular permeability. (C) 2003 Elsevier Science (USA). All rights reserved.