尼古丁通过p38 MAPK信号通路诱导小鼠血管内皮细胞中ICAM-1和VCAM-1的表达

IF 0.1 4区 医学 Q4 Medicine
Hong-Shan Yin, Yong-Jun Li, Zhi-An Jiang, Su-Yun Liu, Bing-Yan Guo, Tao Wang
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引用次数: 0

摘要

目的:探讨吸烟与血栓栓塞事件的关系,探讨吸烟是动脉粥样硬化发病的主要危险因素。研究设计:我们测定了尼古丁对小鼠心脏血管内皮细胞中粘附分子、细胞间粘附分子(ICAM-1)和血管细胞粘附分子(VCAM-1)表达的影响,以及重要的已知中介,即p38丝裂原活化蛋白激酶(MAPK)信号通路的参与。结果:我们的研究结果表明,尼古丁可以通过p38 MAPK信号通路增强小鼠血管内皮细胞中ICAM-1和VCAM-1的表达,导致细胞粘附分子ICAM-1和VCAM-1的表达增加。结论:10(-6)M尼古丁能最大限度地提高小鼠血管内皮细胞ICAM-1和VCAM-1的表达。我们的研究结果提供了尼古丁通过p38 MAPK信号通路刺激这些粘附分子表达的假设机制。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Nicotine-induced ICAM-1 and VCAM-1 expression in mouse cardiac vascular endothelial cell via p38 MAPK signaling pathway.

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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审稿时长
1 months
期刊介绍: AQCH is an Official Periodical of The International Academy of Cytology and the Italian Society of Urologic Pathology.
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