Monocyte chemoattractant protein‐1 (MCP‐1) and interleukin‐8 (IL‐8) are potent chemokines which attract circulating monocytes and neutrophils respectively to inflamed tissues. JE/MCP‐1 gene expression has been previously studied in rabbit aortae after endothelial denudation and the rapid appearance of this transcript was thought to precede emigration of phagocytes. We now report MCP‐1 gene expression following de‐endothelialization of iliac arteries in the pig, a species which can develop spontaneous atherosclerosis. Using Northern blot analysis, we demonstrated that MCP‐1 mRNA was rapidly induced in pig arteries at 2 h and continued to increase to reach a maximum at 8 h before returning to low levels at 16–24 h after injury. The increase seen for MCP‐1 mRNA at 8 h was also observed for IL‐8 mRNA but was not apparent for growth‐related gene expressions, urokinase‐type plasminogen activator (u‐PA), and plasminogen activator inhibitor‐1 (PAI‐1). Since smooth muscle cells, endothelial cells, and phagocytes are all capable of expressing MCP‐1, we examined pig arteries for immunostaining using a monoclonal antibody to human MCP‐1 (5D3‐F7). At 8 h after injury, the predominant cell type staining positive for MCP‐1 was the monocyte/macrophage. Staining was also observed in occasional scattered neutrophils, but MCP‐1 protein could not be detected in smooth muscle cells or on extracellular matrix within the sensitivity constraints posed by our methodology. Our results are consistent with invading monocyte/macrophages having a major input into the production of this chemokine in the arterial wall following injury. The fact that MCP‐1 expression accompanied monocyte/macrophage presence in damaged artery, rather than preceding it, is suggestive that continued MCP‐1 expression is required for functions other than chemoattraction. © 1996 Wiley‐Liss, Inc.