Nicotine-induced ICAM-1 and VCAM-1 expression in mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway.

作者：Hong‐Shan Yin, Yongjun Li, Zhian Jiang, Su-Yun Liu, Bingyan Guo, Tao Wang · 发表于：PubMed · 年份：2014 · 被引用次数：11 · 研究领域：Nicotinic Acetylcholine Receptors Study、Smoking Behavior and Cessation、Vagus Nerve Stimulation Research

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.