期刊
ATHEROSCLEROSIS
卷 237, 期 2, 页码 464-470出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/j.atherosclerosis.2014.10.019
关键词
Vascular smooth muscle; Nicotine; Atherosclerosis; Contractile type; Synthetic type
资金
- Smoking Research Foundation
- Ministry of Education, Culture, Sports, Science and Technology in Japan [23590295]
- Takeda Science Foundation
- Grants-in-Aid for Scientific Research [23590295] Funding Source: KAKEN
Objective: Cigarette smoking is a known risk factor for arteriosclerosis. In atheromatous plaques, vascular smooth muscle cells (VSMCs) display a phenotype that is different from the contractile type under normal conditions. Nicotine is the major pharmacological agent in cigarette smoke. However, any direct effect of nicotine on VSMCs remains uncertain. Because nicotine promotes VSMC migration, its phenotype may change due to nicotine. Approach and results: We used human aorta primary smooth muscle cells (HuAoSMCs), differentiated with transforming growth factor-beta, to investigate changes in the protein levels of differentiation markers and in the activity of mitogen-activated protein kinases (MAPKs) after exposure to 0.1 mu M of nicotine for 48 h. After nicotine exposure, the protein levels of myosin II 10 (2.93-fold) and beta-actin (1.66-fold), synthetic type markers, were increased. In contrast, the levels of the contractile type markers, myosin II 11 (0.63-fold), high-molecular-weight caldesmon (0.40-fold) and SM22 (0.66-fold), which concern differentiated VSMC, were decreased. Moreover, nicotine exposure induced enhanced activation of p38 MAPK (1.30-fold) and extracellular signal-regulated kinase (1.91-fold). These results indicated that the phenotype of HuAoSMCs had changed to a synthetic-like type because of nicotine exposure. Thus, nicotine is one factor that can alter protein expression of differentiation markers in VSMCs. Besides, the increase of intracellular Ca2+ levels suggested that these effects of nicotine were mediated through nicotinic acetylcholine receptors. Conclusion: Nicotine has already been reported to promote VSMC migration from the tunica media to atheromatous plaques in the vascular intima. This phenomenon may occur because nicotine directly induces VSMC transformation from contractile type to synthetic-like type via nicotinic acetylcholine receptors and G protein-coupled receptors. (C) 2014 Elsevier Ireland Ltd. All rights reserved.
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