Motorcycle exhaust particles up-regulate expression of vascular adhesion molecule-1 and intercellular adhesion molecule-1 in human umbilical vein endothelial cells
Motorcycle exhaust particles up-regulate expression of vascular adhesion molecule-1 and intercellular adhesion molecule-1 in human umbilical vein endothelial cells
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DOI：
10.1016/j.tiv.2012.01.021
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发表时间：
2012-06-01
影响因子：
3.2
通讯作者：
Kang, Jaw-Jou
中科院分区：
文献类型：
--
作者：
Lee, Chen-Chen;Huang, Shih-Hsuan;Kang, Jaw-Jou
流行病学研究表明，动脉粥样硬化与环境空气污染之间存在很强的相关性。在这项研究中，我们发现摩托车尾气颗粒（MEP）诱导人单核细胞白血病细胞系（THP-1）与人脐静脉内皮细胞（HUVECs）之间的粘附具有时间和剂量依赖性。此外，MEP处理诱导HUVECs血管细胞粘附分子-1 （VCAM-1）和细胞间粘附分子-1 (ICAM-1) mRNA和蛋白表达。在mep处理的HUVECs中发现I κ B降解和p65核易位，提示核因子κ B （nf - κ B）的参与。NF-kappa B抑制剂BAY 11-7085可抑制mep诱导的VCAM-1和ICAM-1蛋白表达。氧化应激也参与了VCAM-1和ICAM-1表达的信号传导。MEP处理产生过氧化氢和超氧化物。α -生育酚预处理可以抑制mep诱导的活性氧中间体的生成，抑制mep诱导的I κ B降解和粘附分子的表达。此外，不同直径的炭黑纳米颗粒可诱导VCAM-1和ICAM-1蛋白的表达；而多环芳烃（PAHs）在HUVECs中只增加了ICAM-1的表达，而没有增加VCAM-1的表达。在本研究中，我们发现MEPs可以通过氧化应激和NE-kappa B激活诱导HUVECs中ICAM-1和VCAM-1的表达。(C) 2012 Elsevier Ltd.版权所有。
Epidemiological studies have shown that there is a strong correlation between atherosclerosis and ambient air pollution. In this study, we found that motorcycle exhaust particles (MEP) induced adhesion between cells of the human monocytic leukemia cell line (THP-1) and human umbilical vein endothelial cells (HUVECs) in a time-and dose-dependent manner. In addition, MEP treatment induced both mRNA and protein expression of vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) in HUVECs. The I kappa B degradation and p65 nuclear translocation was found in MEP-treated HUVECs, suggested the involvement of nuclear factor-kappa B (NF-kappa B). MEP-induced VCAM-1 and ICAM-1 protein expression was inhibited by NF-kappa B inhibitor BAY 11-7085. Oxidative stress was also involved in the signaling of VCAM-1 and ICAM-1 expression. MEP treatment caused hydrogen peroxide and superoxide formation. Pretreatment with alpha-tocopherol could inhibit MEP-induced reactive oxygen intermediates generation and suppressed MEP-induced I kappa B degradation and adhesion molecules expression. Furthermore, the carbon black (CB) nanoparticles with different diameters could induce VCAM-1 and ICAM-1 protein expression; however, polycyclic aromatic hydrocarbons (PAHs) only increased the expression of ICAM-1 but not that of VCAM-1 in HUVECs. In this study, we found that MEPs could induce ICAM-1 and VCAM-1 expression through oxidative stress and NE-kappa B activation in HUVECs. (C) 2012 Elsevier Ltd. All rights reserved.