Monocyte chemoattractant protein-1 (MCP-1) is a potent chemotactic factor for monocytes, expressed by various cell types including monocytes, vascular endothelial cells, and smooth muscle cells. To investigate the role of MCP-1 in human atherosclerosis, the authors examined 10 normal and 14 diseased human arteries for MCP-1 expression using in situ hybridization. MCP-1 mRNA was detected in 16% of cells counted in human carotid endarterectomy specimens, with the highest expression in organizing thrombi (33%) and macrophage-rich areas bordering the necrotic lipid core (24%). Immunohistochemical staining revealed that MCP-1 mRNA was expressed by vascular smooth muscle cells (VSMCs), mesenchymal appearing intimal cells (MICs), and macrophages. In contrast, few cells expressing MCP-1 mRNA were found in normal arteries (<0.1%). The study also explored the regulation of MCP-1 production by VSMCs in culture, finding that TNFα, gamma interferon (γIFN), and supernatants from mixed lymphocyte cultures increased MCP-1 mRNA levels. These findings suggest that MCP-1 may play a role in mediating monocytic infiltration of the artery wall and that inflammatory mediators can modulate this process.Monocyte chemoattractant protein-1 (MCP-1) is a potent chemotactic factor for monocytes, expressed by various cell types including monocytes, vascular endothelial cells, and smooth muscle cells. To investigate the role of MCP-1 in human atherosclerosis, the authors examined 10 normal and 14 diseased human arteries for MCP-1 expression using in situ hybridization. MCP-1 mRNA was detected in 16% of cells counted in human carotid endarterectomy specimens, with the highest expression in organizing thrombi (33%) and macrophage-rich areas bordering the necrotic lipid core (24%). Immunohistochemical staining revealed that MCP-1 mRNA was expressed by vascular smooth muscle cells (VSMCs), mesenchymal appearing intimal cells (MICs), and macrophages. In contrast, few cells expressing MCP-1 mRNA were found in normal arteries (<0.1%). The study also explored the regulation of MCP-1 production by VSMCs in culture, finding that TNFα, gamma interferon (γIFN), and supernatants from mixed lymphocyte cultures increased MCP-1 mRNA levels. These findings suggest that MCP-1 may play a role in mediating monocytic infiltration of the artery wall and that inflammatory mediators can modulate this process.