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首页> 外文期刊>American Journal of Physiology >Lysophospholipids increase ICAM-1 expression in HUVEC through a Gi- and NF-kappaB-dependent mechanism.
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Lysophospholipids increase ICAM-1 expression in HUVEC through a Gi- and NF-kappaB-dependent mechanism.

机译：溶血磷脂通过Gi和NF-κB依赖性机制增加HUVEC中ICAM-1的表达。

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摘要

Lysophosphatidic acid (LPA) and sphingosine 1-phosphate (S-1-P) are both low molecular weight lysophospholipid (LPL) ligands that are recognized by the Edg family of G protein-coupled receptors. In endothelial cells, these two ligands activate Edg receptors, resulting in cell proliferation and cell migration. The intercellular adhesion molecule-1 (ICAM-1, CD54) is one of many cell adhesion molecules belonging to the immunoglobulin superfamily. This study showed that LPA and S-1-P enhance ICAM-1 expression at both the mRNA and protein levels in human umbilical cord vein endothelial cells (HUVECs). This enhanced ICAM-1 expression in HUVECs was first observed at 2 h postligand treatment. Maximal expression appeared at 8 h postligand treatment, as detected by flow cytometry and Western blotting. Furthermore, the effects of S-1-P on ICAM-1 expression were shown to be concentration dependent. Prior treatment of HUVECs with pertussis toxin, a specific inhibitor of G(i), ammonium pyrrolidinedithiocarbamate andBAY 11-7082, inhibitors of the nuclear factor (NF)-kappaB pathway, or Clostridium difficile toxin B, an inhibitor of Rac, prevented the enhanced effect of LPL-induced ICAM-1 expression. However, pretreatment of HUVECs with exoC3, an inhibitor of Rho, had no effect on S-1-P-enhanced ICAM-1 expression. In a static cell-cell adhesion assay system, pretreatment of LPL enhanced the adhesion between HUVECs and U-937 cells, a human mononucleated cell line. The enhanced adhesion effect could be prevented by preincubation with a functional blocking antibody against human ICAM-1. These results suggest that LPLs released by activated platelets might enhance interactions of leukocytes with the endothelium through a G(i)-, NF-kappaB-, and possibly Rac-dependent mechanism, thus facilitating wound healing and inflammation processes.
机译：溶血磷脂酸（LPA）和鞘氨醇1-磷酸（S-1-P）都是低分子量的溶血磷脂（LPL）配体，它们被G蛋白偶联受体的Edg家族所识别。在内皮细胞中，这两个配体激活Edg受体，导致细胞增殖和细胞迁移。细胞间粘附分子-1（ICAM-1，CD54）是属于免疫球蛋白超家族的许多细胞粘附分子之一。这项研究表明，LPA和S-1-P可以在人脐带静脉内皮细胞（HUVEC）的mRNA和蛋白水平上增强ICAM-1的表达。 HUVEC中这种增强的ICAM-1表达首先在配体处理2小时后观察到。通过流式细胞术和蛋白质印迹检测，在配体处理后8小时出现最大表达。此外，显示S-1-P对ICAM-1表达的影响是浓度依赖性的。 HUVEC预先用百日咳毒素，G（i），吡咯烷二硫代氨基甲酸铵和BAY 11-7082的特异性抑制剂，核因子（NF）-kappaB途径的抑制剂或艰难梭状芽胞杆菌毒素B（Rac的抑制剂）阻止了这种增强作用LPL诱导的ICAM-1表达的影响。然而，用Rho抑制剂exoC3预处理HUVEC对S-1-P增强的ICAM-1表达没有影响。在静态细胞-细胞粘附测定系统中，LPL的预处理可增强HUVEC与人单核细胞系U-937细胞之间的粘附。通过与针对人ICAM-1的功能性封闭抗体进行预温育，可以防止粘附力增强。这些结果表明，活化的血小板释放的LPL可能通过G（i）-，NF-κB和可能的Rac依赖性机制增强白细胞与内皮的相互作用，从而促进伤口愈合和炎症过程。

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