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首页> 外文期刊>Endothelium: Journal of endothelial cell research >Chemokine transport across human vascular endothelial cells.
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Chemokine transport across human vascular endothelial cells.

机译：趋化因子跨人类血管内皮细胞运输。

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摘要

Leukocyte migration across vascular endothelium is mediated by chemokines that are either synthesized by the endothelium or transferred across the endothelium from the tissue. The mechanism of transfer of two chemokines, CXCL10 (interferon gamma-inducible protein [IP]-10) and CCL2 (macrophage chemotactic protein [MCP]-1), was compared across dermal and lung microvessel endothelium and saphenous vein endothelium. The rate of transfer depended on both the type of endothelium and the chemokine. The permeability coefficient (Pe) for CCL2 movement across saphenous vein was twice the value for dermal endothelium and four times that for lung endothelium. In contrast, the Pe value for CXCL10 was lower for saphenous vein endothelium than the other endothelia. The differences in transfer rate between endothelia was not related to variation in paracellular permeability using a paracellular tracer, inulin, and immunoelectron microscopy showed that CXCL10 was transferred from the basal membrane in a vesicular compartment, before distribution to the apical membrane. Although all three endothelia expressed high levels of the receptor for CXCL10 (CXCR3), the transfer was not readily saturable and did not appear to be receptor dependent. After 30 min, the chemokine started to be reinternalized from the apical membrane in clathrin-coated vesicles. The data suggest a model for chemokine transcytosis, with a separate pathway for clearance of the apical surface.
机译：跨血管内皮的白细胞迁移是由趋化因子介导的，趋化因子由内皮合成或从组织跨过内皮转移。比较了两种趋化因子CXCL10（干扰素γ诱导蛋白[IP] -10）和CCL2（巨噬细胞趋化蛋白[MCP] -1）在皮肤，肺微血管内皮和大隐静脉内皮中的转移机制。转移速率取决于内皮的类型和趋化因子。 CCL2在大隐静脉中移动的渗透系数（Pe）是真皮内皮细胞的两倍，是肺内皮细胞的四倍。相反，大隐静脉内皮细胞的CXCL10的Pe值低于其他内皮细胞。使用细胞旁示踪剂，菊粉和免疫电子显微镜观察，内皮细胞之间的转移速率差异与细胞旁通透性的变化无关，免疫电子显微镜显示，CXCL10在分配至顶膜之前从囊泡隔室的基底膜转移。尽管所有三个内皮细胞均表达高水平的CXCL10受体（CXCR3），但转移并不容易饱和，并且似乎不依赖受体。 30分钟后，趋化因子开始从网格蛋白包被的囊泡的顶端膜中重新趋化。数据提示了趋化因子转胞作用的模型，其具有清除顶表面的单独途径。

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