Nicotine-induced upregulation of VCAM-1, MMP-2, and MMP-9 through the α7-nAChR-JNK pathway in RAW264.7 and MOVAS cells

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• 作者：Zong-Zhuang Li (1) (2)
  Zhen-Zhen Guo (1)
  Zhi Zhang (1)
  Qun-An Cao (1)
  Ya-Juan Zhu (1)
  Hua-Li Yao (1)
  Li-Li Wu (1)
  Qiu-Yan Dai (1)
  
• 关键词：Nicotine ; JNK ; Nicotinic acetylcholine receptors ; Vascular cell adhesion molecular ; Matrix metalloproteinase
• 刊名：Molecular and Cellular Biochemistry
• 出版年：2015
• 出版时间：January 2015
• 年：2015
• 卷：399
• 期：1-2
• 页码：49-58
• 全文大小：2,287 KB
• 参考文献：1. Wang S, Zhang C, Zhang M, Liang B, Zhu H, Lee J, Viollet B, Xia L, Zhang Y, Zou MH (2012) Activation of AMP-activated protein kinase alpha2 by nicotine instigates formation of abdominal aortic aneurysms in mice in vivo. Nat Med 18:902-10. doi:10.1038/nm.2711 CrossRef
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  11. Lau PP, Li L, Merched AJ, Zhang AL, Ko KW, Chan L (2006) Nicotine induces proinflammatory responses in macrophages and the aorta leading to acceleration of atherosclerosis in low-density lipoprotein receptor(-/-) mice. Arterioscler Thromb Vasc Biol 26:143-49. doi:10.1161/01.ATV.0000193510.19000.10 CrossRef
  12. Yoshimura K, Aoki H, Ikeda Y, Fujii K, Akiyama N, Furutani A, Hoshii Y, Tanaka N, Ricci R, Ishihara T, Esato K, Hamano K, Matsuzaki M (2005) Regression of abdominal aortic aneurysm by inhibition of c-Jun N-terminal kinase. Nat Med 11:1330-338. doi:10.1038/nm1335 CrossRef
  13. Dimu
• 作者单位：Zong-Zhuang Li (1) (2)
  Zhen-Zhen Guo (1)
  Zhi Zhang (1)
  Qun-An Cao (1)
  Ya-Juan Zhu (1)
  Hua-Li Yao (1)
  Li-Li Wu (1)
  Qiu-Yan Dai (1)
  
  1. Department of Cardiology, Shanghai First People’s Hospital, School of Medicine, Shanghai Jiao Tong University, Shanghai, 200080, China
  2. Department of Cardiology, Guizhou Provincial People’s Hospital, Guiyang, 550002, China
  
• ISSN：1573-4919

文摘

The ability of nicotine to induce aortic aneurysms has been shown in animal models; however, its underlying mechanisms remain elusive. In the present experiment, both the RAW264.7 and MOVAS cell lines were employed to examine the nicotine-induced modulation of VCAM-1, MMP-2, and MMP-9 expressions in macrophages and vascular smooth muscle cells. Our results showed that nicotine concentrations of both 0.5 and 5?ng/ml induced VCAM-1, MMP-2, and MMP-9 upregulation, while a concentration of 50?ng/ml had a slight inhibitory effect and a concentration of 500?ng/ml showed a significant inhibitory effect. When cells were pretreated with either SP600125 (JNK inhibitor) or PNU-282987 (α7-nAChR agonist) prior to nicotine exposure, the nicotine-induced upregulation of VCAM-1, MMP-2, MMP-9, and p-JNK was suppressed, with a joint treatment producing a more significant inhibitory effect. Moreover, PNU-282987 had a comparable inhibitory effect on VCAM-1, MMP-2, and MMP-9 expressions and JNK activation via phosphorylation as did SP600125. In conclusion, nicotine-induced VCAM-1, MMP-2, and MMP-9 expressions occur in a dose-dependent fashion in both of the cell lines tested. Furthermore, the nicotine exposure equivalent to plasma levels found in regular smokers can augment VCAM-1, MMP-2, and MMP-9 expressions through the α7-nAChR-JNK pathway.