Objective: To explore the link between cigarette smoking and thromboembolic events and to investigate cigarette smoking as a major risk factor in the etiology of atherosclerosis.
Study Design: We determined the effect of nicotine on the expression of adhesion molecules, intercellular adhesion molecule (ICAM-1), and vascular cell adhesion molecule (VCAM-1) in mouse cardiac vascular endothelial cells and the involvement of important known intermediaries, namely p38 mitogen-activated protein kinase (MAPK) signaling pathway.
Results: Our results indicate that nicotine can enhance the expression of ICAM-1 and VCAM-1 on mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway, resulting in increased expression of the cellular adhesion molecules ICAM-1 and VCAM-1.
Conclusion: We demonstrate that 10(-6) M nicotine maximally enhances mouse cardiac vascular endothelial cell expression of ICAM-1 and VCAM-1 at 8 hours. Our results provide a putative mechanism by which nicotine stimulates expression of these adhesion molecules via p38 MAPK signaling pathway.
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