High-shear-stress-induced activation of platelets and microparticles enhances expression of cell adhesion molecules in THP-1 and endothelial cells
High-shear-stress-induced activation of platelets and microparticles enhances expression of cell adhesion molecules in THP-1 and endothelial cells
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DOI：
10.1016/s0021-9150(01)00433-6
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发表时间：
2001-10-01
期刊：
影响因子：
5.3
通讯作者：
Kambayashi, J
中科院分区：
文献类型：
--
作者：
Nomura, S;Tandon, NN;Kambayashi, J
白细胞与内皮细胞(ECs)之间的相互作用对于体内血管内稳态和有效的免疫炎症反应是必不可少的。血小板衍生微粒(PMPs)是在高剪应力作用下产生的，在各种临床情况下可出现在病变的小动脉和小动脉中。在本研究中，我们利用流式细胞术和激光共聚焦扫描显微镜研究了高切诱导的血小板和微粒子激活对THP-1和内皮细胞黏附分子的影响。我们还检测了PMP刺激后THP-1和ECs产生的一些细胞因子，并研究了细胞因子mRNA的表达。PMP刺激THP-1细胞增加CD11b、CD32和CD33，但不增加CD29、CD31和CD36。PMP刺激内皮细胞可增加CD54和CD63，但不增加CD9、CD29和CD31。PMPs诱导THP-1产生白介素8(IL-8)、白介素1β(IL-1β)和肿瘤坏死因子α(TNFα)。PMPs还可诱导内皮细胞产生IL-8、IL-1β和IL-6。生产是依赖时间的。逆转录-聚合酶链式反应检测到PMP刺激后THP-1和ECs中一些细胞因子的mRNAs。与PMP刺激后的黏附有关，我们不仅可以清楚地观察到CD11b在THP-1细胞中的分布，而且可以观察到CD54在ECs中的分布发生了变化。此外，抗P-选择素糖蛋白配体-1抗体还降低了PMP刺激后THP-1中CD11b、CD32和CD33的表达。这些结果表明，高切变诱导的微粒可能参与了动脉粥样硬化的发展，并参与了炎性疾病中的血管损伤。(C)2001爱思唯尔爱尔兰科学有限公司。保留所有权利。
Interaction between leukocyte and endothelial cells (ECs) is essential for vascular homeostasis and competent immune-inflammatory responses in vivo. Platelet-derived microparticles (PMPs) are generated by high shear stress and may appear in diseased small arteries and arterioles in various clinical settings. In this study, we used flow cytometry and confocal laser scanning microscopy to investigate the effects of high-shear-induced platelet and microparticle activation in adhesion molecules of THP-1 and ECs. We also measured the production of some cytokines and studied cytokine mRNA from THP-1 and ECs after PMP stimulation. PMP stimulation of THP-1 cells increased CD11b, CD32, and CD33 but not CD29, CD31, and CD36. PMP stimulation of ECs increased CD54 and CD63 but not CD9, CD29, and CD31. PMPs induced interleukin-8 (IL-8), interleukin-1 beta (IL-1 beta), and tumor necrosis factor alpha (TNF alpha) production by THP-1. PMPs also induced IL-8, IL-1 beta, and interleukin-6 (IL-6) production by ECs. Production was time-dependent. With RT-PCR, some cytokine mRNAs were detected in THP-1 and ECs after PMP stimulation. In relation to adhesiveness after PMP stimulation, we could clearly observe a shift in distribution not only of CD11b in THP-1 cells but also of CD54 in ECs. In addition, anti-P-selectin glycoprotein ligand-1 antibody reduced the expression of CD11b, CD32, and CD33 in THP-1 after PMP stimulation. These results suggest that high-shear-induced microparticles may contribute to the development of atherosclerosis and participate in vascular damage in inflammatory disorders. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.