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首页> 外文期刊>Journal of Cellular Physiology >Opposing effect of angiopoietin-1 on VEGF-mediated disruption of endothelial cell-cell interactions requires activation of PKCbeta.
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Opposing effect of angiopoietin-1 on VEGF-mediated disruption of endothelial cell-cell interactions requires activation of PKCbeta.

机译：反对的影响而VEGF-mediated破坏内皮和信息交互需要激活PKCbeta。

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Angiopoietin-1 (Ang1) and vascular endothelial growth factor (VEGF) cooperate in migration and survival of endothelial cells by activation of phosphatidylinositol-3 (PI-3) kinase and mitogen activating protein (MAP) kinase pathways. However, Ang1 opposes the effect of VEGF on vascular permeability. We found that Ang1 also blocks VEGF-mediated diffusion of fluoresin isothiocyanate (FITC)-labeled albumin across an endothelial cell monolayer. VEGF-mediated vascular permeability has been attributed, in part, to activation of phospholipase A(2) and subsequent formation of platelet activating factor. However, Ang1 had no effect on VEGF-induced activation of phospholipase A(2) or the release of arachidonic acid. VEGF-mediated permeability was associated with disruption of endothelial cell junctional complexes, dissociation of beta-catenin from VE-cadherin, and accumulation of beta-catenin in the cytosol. In contrast, Ang1 enhanced the interaction of beta-catenin with VE-cadherin and impaired VEGF-mediated dissociation of this complex. Ang1 also blocked VEGF-induced translocation of protein kinase C (PKC) and beta2 to the membrane, but had no effect on activation of PKCalpha. In addition, staurosporine and a PKCbeta inhibitor, LY379196, blocked VEGF-mediated dissociation of beta-catenin from VE-cadherin, diffusion of albumin across the endothelial cell monolayer, and translocation of PKCbeta isoforms. These data indicate that VEGF-mediated disruption of endothelial cell-cell interactions requires activation of PKCbeta isoforms and that this pathway is blocked by Ang1. J. Cell. Physiol. 198: 53-61, 2004.
机译：而(Ang1)和血管内皮生长因子(VEGF)在迁移和合作激活的内皮细胞的生存phosphatidylinositol-3 (PI-3)激酶和有丝分裂原激活蛋白激酶通路(图)。然而,Ang1反对VEGF的影响血管通透性。块VEGF-mediated fluoresin扩散在一个异硫氰酸酯(FITC)标记的白蛋白内皮细胞单层。由于血管通透性,部分激活磷脂酶(2)和随后形成的血小板激活的因素。VEGF-induced激活磷脂酶(2)或花生四烯酸的释放。渗透率与中断相关内皮细胞联接的复合物,从VE-cadherinβ-连环蛋白的分离,和β-连环蛋白细胞溶质的积累。相比之下,Ang1增强的相互作用β-连环蛋白VE-cadherin和受损VEGF-mediated离解的复杂。也阻止了VEGF-induced易位蛋白激酶C (PKC)和beta2膜,但对激活PKCalpha没有影响。此外,staurosporine和PKCbeta抑制剂,LY379196,阻塞VEGF-mediated离解β-连环蛋白从VE-cadherin扩散白蛋白在内皮细胞单层,和易位PKCbeta亚型。表明VEGF-mediated破坏内皮和信息交互的需要激活PKCbeta亚型,这通路被Ang1。198: 53-61, 2004.

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