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Research Article Free access | 10.1172/JCI117761
3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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3rd Department of Internal Medicine, Faculty of Medicine, University of Tokyo, Japan.
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Published March 1, 1995 - More info
Vascular medial smooth muscle cells migrate, proliferate and transform to foam cells in the process of atherosclerosis. We have reported that the intimal smooth muscle cells express proto-oncogene c-fms, a characteristic gene of monocyte-macrophages, which is not normally expressed in medial smooth muscle cells. In the present study, we demonstrated that combinations of platelet-derived growth factor (PDGF)-BB and either epidermal growth factor (EGF) or fibroblast growth factor (FGF) induced high expression of c-fms in normal human medial smooth muscle cells to the level of intimal smooth muscle cells or monocyte-derived macrophages, whereas c-fms expression by PDGF-BB alone was 1/10 and both EGF and FGF had no independent effect on c-fms expression. By contrast, interferon (IFN)-gamma and macrophage colony-stimulating factor (M-CSF) suppressed the induction of c-fms expression. These results indicate that multiple growth factors and cytokines may play a role in the phenotypic transformation of medial smooth muscle cells to intimal smooth muscle cells in atherosclerotic lesions by altering c-fms expression.
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