Journal
TOXICOLOGY IN VITRO
Volume 26, Issue 4, Pages 552-560Publisher
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.tiv.2012.01.021
Keywords
Motorcycle exhaust particle; Polycyclic aromatic hydrocarbons; Cell adhesion molecule; Oxidative stress; NF-kappa B
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Funding
- Taiwan National Science Council [NSC93-2320-B002-118]
- China Medical University in Taiwan [CMU 99-S-28, CMU100-S-12]
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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.
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