血小板红蛋白维持血管内皮细胞连接的完整性并调节vegf诱导的ve -钙粘蛋白磷酸化

F. Muramatsu, H. Kidoya, Hisamichi Naito, Yumiko Hayashi, Tomohiro Iba, N. Takakura
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引用次数: 13

摘要

血小板红蛋白,也被称为γ-连环蛋白,是β-连环蛋白的密切同源物,并与共享的蛋白伴侣相互作用。β-catenin在细胞粘附中的功能是通过与血管内皮(VE)-钙粘蛋白相互作用来维持内皮屏障功能。血小板红蛋白也与ve -钙粘蛋白相互作用,但其在细胞粘附中的作用尚不清楚。在这里,我们研究了血小板红蛋白在血管内皮细胞(ECs)-细胞连接完整性中的功能。敲低ECs中血小板红蛋白的表达并不会阻止细胞增殖或细胞迁移,但会导致ve -钙粘蛋白膜分布的不稳定,导致通透性增加。在稳定状态下,血小板蛋白有助于VE-cadherin依赖性粘附,但在血管内皮生长因子(VEGF)的刺激下,它是诱导VEGF信号上VE-cadherin磷酸化的必要条件,从而破坏细胞-细胞连接的稳定。此外,敲除血小板红蛋白表达增加血管内皮蛋白酪氨酸磷酸酶活性,这是一种与ve -钙粘蛋白相关的内皮特异性膜蛋白。这些结果表明,血小板红蛋白在细胞-细胞粘附的调节中以一种环境依赖的方式发挥多种作用。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Plakoglobin maintains the integrity of vascular endothelial cell junctions and regulates VEGF-induced phosphorylation of VE-cadherin
Plakoglobin, also known as γ-catenin, is a close homolog of β-catenin and interacts with shared protein partners. Functions of β-catenin in cell adhesion are well-documented in terms of maintaining endothelial barrier function by interacting with vascular endothelial (VE)-cadherin. Plakoglobin also interacts with VE-cadherin, but its function in cell adhesion is not well understood. Here, we investigated plakoglobin function in vascular endothelial cell (ECs)-cell junction integrity. Knock-down of plakoglobin expression in ECs did not prevent cell proliferation or cell migration, but induced destabilization of the membrane distribution of VE-cadherin and resulted in increased permeability. Plakoglobin contributes to VE-cadherin-dependent adhesion in the steady state, but on stimulation with vascular endothelial growth factor (VEGF), it is essential for inducing sufficient VE-cadherin phosphorylation on VEGF signaling, thereby destabilizing cell-cell junctions. Furthermore, knock-down of plakoglobin expression increased vascular endothelial protein tyrosine phosphatase activity, an endothelial-specific membrane protein associating with VE-cadherin. These results indicate that plakoglobin plays multiple roles in regulation of cell-cell adhesion in a context dependent manner.
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