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首页> 外文期刊>Journal of Cellular Physiology >Antagonistic effect of NK4 on HGF/SF induced changes in the transendothelial resistance (TER) and paracellular permeability of human vascular endothelial cells.
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Antagonistic effect of NK4 on HGF/SF induced changes in the transendothelial resistance (TER) and paracellular permeability of human vascular endothelial cells.

机译：敌对的NK4 HGF / SF诱导的影响transendothelial阻力的变化(TER)和paracellular人类血管的渗透性内皮细胞。

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摘要

Hepatocyte growth factor/scatter factor (HGF/SF) is a multi-function cytokine that has been shown to regulate the expression of cell adhesion molecules in human endothelial cells. It is also a key cytokine in the development and progression of cancer, particularly during metastasis. NK4 is a variant of HGF/SF that has already been shown to be antagonistic to HGF/SF. This study shows that HGF/SF decreased transendothelial resistance (TER) and increased paracellular permeability in human vascular endothelial cells can that such effects can be inhibited by addition of the NK4 variant. In addition, HGF/SF-stimulated invasion of endothelium by breast cancer cells was inhibited by the addition of NK4. Western blotting revealed that HGF/SF decreased the protein level, and increased tyrosine phosphorylation of ZO-1, but did not cause a change in level of occludin or claudin-1, both molecules involved in tight junction function. RT-PCR revealed that addition of HGF/SF caused no change in signal for claudin-5 or junctional adhesion molecule (JAM), but there was a decrease in the signal for claudin-1. NK4 was able to prevent the decrease in levels of ZO-1 protein by HGF/SF. Copyright 2002 Wiley-Liss, Inc.
机译：肝细胞生长因子/散射因子(HGF / SF)是一种多功能细胞因子,已被证明吗调节细胞粘附的表达分子在人类内皮细胞。一个关键细胞因子的开发和发展癌症,特别是在转移。HGF / SF的变种已经被证明敌对的HGF / SF。HGF / SF transendothelial减少阻力(TER)和paracellular渗透性增加人血管内皮细胞可以这样可以通过添加NK4抑制效果变体。内皮的乳腺癌细胞添加NK4抑制。印迹显示HGF / SF的下降蛋白质水平,增加酪氨酸磷酸化ZO-1,但没有引起occludin或claudin-1水平变化的分子参与紧密连接功能。rt - pcr显示添加HGF / SF没有造成的信号变化claudin-5或交界粘附分子(果酱),但有一个减少claudin-1信号。防止ZO-1蛋白水平的降低HGF / SF。

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