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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Differential induction of BLT receptor expression on human endothelial cells by lipopolysacharide, cytokines, and leukotriene B-4
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Differential induction of BLT receptor expression on human endothelial cells by lipopolysacharide, cytokines, and leukotriene B-4

机译：脂多糖，细胞因子和白三烯B-4对人内皮细胞BLT受体表达的差异诱导

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摘要

Leukotriene (LT) B-4 is a powerful chemotactic and immune modulating agent that signals via two receptors denoted BLT1 and BLT2. Here we report that BLT1 and BLT2 are expressed at low levels in an apparently silent state in human umbilical vein endothelial cells (HUVEC). However, treatment with LPS leads to a > 10 fold increase in the levels of BLT1 mRNA without any significant effects on BLT2 mRNA. In parallel, LIPS also increases the amounts of BLT1 protein. Tumor necrosis factor-alpha (TNF-alpha) increases the expression of BLT2 mRNA approximate to 6 times above basal levels with only a modest increase in BLT1 mRNA. Interleukin-1 beta causes variable and parallel increases of both BLT1 and BLT2 mRNA. The natural ligand LTB4 also increases BLT1, but not BLT2, mRNA and protein expression. Along with the induction of BLT1 and/or BLT2, HUVEC acquire the capacity to respond to LTB4 with increased levels of intracellular calcium and these signals can be blocked by isotype selective BLT antagonists, CP-105696 and LY-255283. In addition, treatment of HUVEC with LTB4 causes increased release of both nitrite, presumably reflecting nitric oxide (NO), and monocyte chemoattractant protein-1. Our data indicate that expression of functional BLT receptors may occur at the surface of endothelial cells in response to LIPS, cytokines, and ligand, which in turn may have functional consequences during the early vascular responses to inflammation. Moreover, the results point to BLT receptors as potential targets for pharmacological intervention in LT-dependent inflammatory diseases such as asthma, rheumatoid arthritis, and arteriosclerosis.
机译：白三烯（LT）B-4是一种强大的趋化性和免疫调节剂，可通过两个受体BLT1和BLT2发出信号。在这里我们报告说，BLT1和BLT2在人类脐静脉内皮细胞（HUVEC）中以低水平表达，且处于明显沉默状态。但是，用LPS进行治疗会导致BLT1 mRNA水平增加> 10倍，而对BLT2 mRNA却没有任何明显影响。同时，LIPS还增加了BLT1蛋白的含量。肿瘤坏死因子-α（TNF-alpha）使BLT2 mRNA的表达比基础水平高约6倍，而BLT1 mRNA仅适度增加。白介素-1β引起BLT1和BLT2 mRNA的可变和平行增加。天然配体LTB4也增加BLT1，但不增加BLT2，mRNA和蛋白质表达。随着BLT1和/或BLT2的诱导，HUVEC获得了通过增加细胞内钙水平来响应LTB4的能力，并且这些信号可以被同型选择性BLT拮抗剂CP-105696和LY-255283阻断。此外，用LTB4处理HUVEC会导致亚硝酸盐（可能反映一氧化氮（NO））和单核细胞趋化蛋白1的释放增加。我们的数据表明，功能性BLT受体的表达可能会响应LIPS，细胞因子和配体而出现在内皮细胞表面，进而在早期血管对炎症的反应中可能产生功能性后果。此外，研究结果表明，BLT受体可能是针对LT依赖性炎症性疾病（例如哮喘，类风湿性关节炎和动脉硬化）进行药理干预的潜在靶标。

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