MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury
Copyright policy )MCP-1 deficiency is associated with reduced intimal hyperplasia after arterial injury
Monocyte chemoattractant protein (MCP)-1 is abundant in smooth muscle cells (SMC) and macrophages of atherosclerotic plaques and in the injured arterial wall. MCP-1 and its receptor, CCR2, are important mediators of macrophage accumulation and atherosclerotic plaque progression. We have recently reported that CCR2(-/-) mice have a approximately 60% decrease in intimal hyperplasia and medial DNA synthesis in response to femoral arterial injury. We have now examined the response to femoral arterial injury in MCP-1(-/-) mice. MCP-1 deficiency was associated with a approximately 30% reduction in intimal hyperplasia at 4 weeks and was not associated with diminished medial DNA synthesis. Despite inducing tissue factor in SMC culture, MCP-1 deficiency was not associated with a decrease in neointimal tissue factor after injury. These data suggest that MCP-1 and CCR2 deficiencies have distinct effects on arterial injury. The effects of MCP-1 on intimal hyperplasia may be mediated largely through SMC migration.
- Brigham and Women's Faulkner Hospital United States
- Icahn School of Medicine at Mount Sinai United States
- Harvard University United States
- Dana-Farber Cancer Institute United States
Hyperplasia, Receptors, CCR2, Macrophages, Mice, Transgenic, Muscle, Smooth, Arteries, DNA, Immunohistochemistry, Femoral Artery, Mice, Bromodeoxyuridine, Cell Movement, Animals, Receptors, Chemokine, Chemokines, Tunica Intima, Cell Division, Chemokine CCL2
Hyperplasia, Receptors, CCR2, Macrophages, Mice, Transgenic, Muscle, Smooth, Arteries, DNA, Immunohistochemistry, Femoral Artery, Mice, Bromodeoxyuridine, Cell Movement, Animals, Receptors, Chemokine, Chemokines, Tunica Intima, Cell Division, Chemokine CCL2
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