These authors contributed equally to this article.
Recombinant human CXCL8(3-72)K11R/G31P regulates smooth muscle cell proliferation and migration through blockage of interleukin-8 receptor
Article first published online: 24 DEC 2012
Copyright © 2012 International Union of Biochemistry and Molecular Biology, Inc.
Special Issue: Biointeractomics: A Mini-Theme Issue
Volume 65, Issue 1, pages 67–75, January 2013
How to Cite
Qin, Y., Fan, F., Zhao, Y., Cui, Y., Wei, X., Kohama, K., Gordon, J. R., Li, F. and Gao, Y. (2013), Recombinant human CXCL8(3-72)K11R/G31P regulates smooth muscle cell proliferation and migration through blockage of interleukin-8 receptor. IUBMB Life, 65: 67–75. doi: 10.1002/iub.1107
- Issue published online: 24 DEC 2012
- Article first published online: 24 DEC 2012
- Manuscript Accepted: 2 OCT 2012
- Manuscript Received: 17 JUL 2012
- vascular smooth muscle cell
Atherosclerosis is a chronic inflammatory disease with multiple contributing factors. Hyperlipidemia is one of the major independent risks, and interleukin-8 (IL-8), as an inflammatory factor, plays an important role in the development of atherosclerosis. The aims of the study were to examine the therapeutic efficacy of G31P, an antagonist of IL-8 receptor, with a mouse model of hyperlipidemia and the potential mechanisms of G31P through the vascular smooth muscle cell (VSMC) proliferation and migration in a cell line. In vivo study: Male BALB/c mice were fed a high-fat diet for 6 months. G31P was injected subcutaneously. Blood keratinocyte chemoattractant, lipid profile, and aorta expression of inflammatory factors, matrix metalloproteinases, MMP2 and MMP9 were investigated. In vitro study: A7R5 cells were treated with IL-8 with/without G31P. Cell proliferation and migration were investigated. G31P significantly suppressed the hyperlipidermia-induced abnormal lipid profile and increased IL-8, proinflammatory factor, MMP2 and MMP9 expression. G31P also inhibited VSMC proliferation and migration both in vitro and in vivo. These findings indicate the potential therapeutic effects of G31P in preventing the development of atherosclerosis by antagonizing IL-8 receptor and decreasing the biologic activity of IL-8. © 2012 IUBMB Life, 65(1):67–75, 2013