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首页> 外文期刊>Biochimica et biophysica acta. Molecular basis of disease: BBA >CXCR4 on human endothelial cells can serve as both a mediator of biological responses and as a receptor for HIV-2
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CXCR4 on human endothelial cells can serve as both a mediator of biological responses and as a receptor for HIV-2

机译：人内皮细胞上的CXCR4既可以充当生物反应的介质，又可以充当HIV-2的受体

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It has been shown that deletion of the chemokine receptor, CXCR4, causes disordered angiogenesis in mouse models. In the present studies, we examined the distribution and trafficking of CXCR4 in human endothelial cells, tested their responses to the CXCR4 ligand, SDF-1, and asked whether endothelial cell CXCR4 can serve as a cell surface receptor for the binding of viruses. The results show that CXCR4 is present on endothelial cells from coronary arteries, iliac arteries and umbilical veins (HUVEC), but expression was heterogeneous, with some cells expressing CXCR4 on their surface, while others did not. Addition of SDF-1 caused a rapid decrease in CXCR4 surface expression. It also caused CXCR4-mediated activation of MAPK, release of PGI_2, endothelial migration, and the formation of capillary-like structures by endothelial cells in culture. Co-culture of HUVEC with lymphoid cells that were chronically infected with a CD4-independent/CXCR4-tropic variant of HIV-2 resulted in the formation of multinucleated syncytia. Formation of the syncytia was inhibited by each of several different CXCR4 antibodies. Thus, our findings indicate: (1) that CXCR4 is widely expressed on human endothelial cells; (2) the CXCR4 ligand, SDF-1, can evoke a wide variety of responses from human endothelial cells; and (3) CXCR4 on endothelial cells can serve as a receptor for isolates of HIV that can utilize chemokine receptors in the absence of endothelial cells can serve as a receptor for isolates of HIV that can utilize chemokine receptors in the absence of CD4.
机译：已经显示趋化因子受体CXCR4的缺失引起小鼠模型中血管生成的紊乱。在本研究中，我们检查了CXCR4在人内皮细胞中的分布和运输，测试了它们对CXCR4配体SDF-1的反应，并询问内皮细胞CXCR4是否可以充当病毒结合的细胞表面受体。结果表明，CXCR4存在于冠状动脉，动脉和脐静脉（HUVEC）的内皮细胞中，但表达是异质的，一些细胞在其表面表达CXCR4，而其他细胞则不表达。 SDF-1的添加导致CXCR4表面表达迅速下降。它也引起CXCR4介导的MAPK活化，PGI_2释放，内皮迁移以及培养中的内皮细胞形成毛细血管样结构。 HUVEC与长期感染HIV-2 CD4 / CXCR4嗜性变体的淋巴样细胞的共培养导致形成多核合胞体。几种不同的CXCR4抗体均抑制合胞体的形成。因此，我们的发现表明：（1）CXCR4在人内皮细胞上广泛表达; （2）CXCR4配体SDF-1可以引起人内皮细胞的多种应答; （3）内皮细胞上的CXCR4可以用作在没有内皮细胞的情况下可以利用趋化因子受体的HIV分离株的受体，而在没有CD4的情况下可以作为利用趋化因子受体的HIV分离株的受体。

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