Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:914-920
Published online before print April 18, 2002, doi: 10.1161/01.ATV.0000019009.73586.7F
Published online before print April 18, 2002, doi: 10.1161/01.ATV.0000019009.73586.7F
© 2002 American Heart Association, Inc.
Vascular Biology |
Monocyte Chemoattractant Protein-1 Induces Proliferation and Interleukin-6 Production in Human Smooth Muscle Cells by Differential Activation of Nuclear Factor-
B and Activator Protein-1
From Innere Medizin III (C.V., J.V., T.A., W.S., W.K., J.K.) Universität Heidelberg, Germany, and Innere Medizin, Abteilung für Nephrologie/ Hypertonie, (S.R.O.), Inselspital, Bern, Switzerland.
Correspondence to Dr J. Kreuzer, Innere Medizin III, Universität Heidelberg, Bergheimer Str. 58, 69115 Heidelberg, Germany. E-mail joerg_kreuzer{at}med.uni-heidelberg.de
Abstract— Inflammatory response and chemotaxis of vascular wall cells play an important pathogenic role in the development of atherosclerosis. Monocyte chemoattractant protein-1 (MCP-1) is a potent chemoattractant for monocytes. Besides the induction of monocyte recruitment, it has been suggested that MCP-1 may directly activate smooth muscle cells. We investigated whether MCP-1 affects the proliferation and cytokine production of human vascular smooth muscle cells (VSMCs) and determined the underlying signal transduction pathways. Stimulation of VSMCs with MCP-1 induced proliferation and resulted in a concentration- and time-dependent release of the proinflammatory cytokine interleukin-6 (IL-6). Pretreatment with pertussis toxin, GF109203X, and pyrrolidine dithiocarbamate inhibited MCP-1–dependent IL-6 release, suggesting the involvement of Gi proteins, protein kinase C, and nuclear factor-
B (NF-B). MCP-1 also induced extracellular signal–regulated kinase, which, along with IL-6 release, was inhibited by pertussis toxin. PD98059 prevented MCP-1–induced extracellular signal–regulated kinase activation and cell proliferation. MCP-1 stimulated the binding activity of NF-B and of activator protein-1 (AP-1). As demonstrated by cis element double-stranded (decoy) oligodeoxynucleotides, NF-B was involved in IL-6 release by MCP-1, whereas proliferation was dependent on AP-1. The results clearly demonstrate that MCP-1 induces differential activation of NF-B and AP-1 in VSMCs. Thus, our data propose a new mechanism for the proatherogenic effect of MCP-1.
Key Words: atherosclerosis • monocyte chemoattractant protein-1 • interleukin-6 • nuclear factor-B • activator protein-1
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