Monocyte chemoattractant protein-1 (MCP-1) is a chemotactic molecule expressed by monocytes, vascular endothelial cells, and smooth muscle cells. This study investigated MCP-1 expression in human atheromatous plaques using in situ hybridization. MCP-1 mRNA was detected in 16% of 10,768 cells in atheroma, with highest expression in organizing thrombi (33%) and macrophage-rich areas (24%), compared to the fibrous cap (8%) and necrotic lipid core (5%). MCP-1 was expressed by vascular smooth muscle cells (VSMC), mesenchymal appearing intimal cells (MICs), and macrophages. In contrast, normal arteries showed minimal expression (<0.1%). These findings suggest a potential role for MCP-1 in mediating monocytic infiltration into the artery wall. In vitro studies showed that cytokines such as TNFα, γIFN, and supernatants from mixed lymphocyte cultures increased MCP-1 mRNA levels in cultured endothelial cells and fibroblasts. In vivo, MCP-1 was produced by macrophages, VSMCs, and MICs in atherosclerotic plaques. MCP-1 expression by VSMCs was stimulated by TNFα and γIFN. These results suggest that MCP-1 may play a role in the recruitment of monocytes to the vessel wall in atherosclerosis. The study also highlights the potential of MCP-1 as a mediator in the progression of atherosclerosis, with implications for future therapeutic strategies targeting MCP-1.Monocyte chemoattractant protein-1 (MCP-1) is a chemotactic molecule expressed by monocytes, vascular endothelial cells, and smooth muscle cells. This study investigated MCP-1 expression in human atheromatous plaques using in situ hybridization. MCP-1 mRNA was detected in 16% of 10,768 cells in atheroma, with highest expression in organizing thrombi (33%) and macrophage-rich areas (24%), compared to the fibrous cap (8%) and necrotic lipid core (5%). MCP-1 was expressed by vascular smooth muscle cells (VSMC), mesenchymal appearing intimal cells (MICs), and macrophages. In contrast, normal arteries showed minimal expression (<0.1%). These findings suggest a potential role for MCP-1 in mediating monocytic infiltration into the artery wall. In vitro studies showed that cytokines such as TNFα, γIFN, and supernatants from mixed lymphocyte cultures increased MCP-1 mRNA levels in cultured endothelial cells and fibroblasts. In vivo, MCP-1 was produced by macrophages, VSMCs, and MICs in atherosclerotic plaques. MCP-1 expression by VSMCs was stimulated by TNFα and γIFN. These results suggest that MCP-1 may play a role in the recruitment of monocytes to the vessel wall in atherosclerosis. The study also highlights the potential of MCP-1 as a mediator in the progression of atherosclerosis, with implications for future therapeutic strategies targeting MCP-1.