Induction of IG9 monocyte adhesion molecule expression in smooth muscle and endothelial cells after balloon arterial injury in cholesterol-fed rabbits

The expression of monocyte-specific adhesion molecules and chemokines by ce ll types within the vessel wall plays an important role in foam cell accumu lation during atherosclerotic plaque development. We previously identified IG9, a novel monocyte adhesion protein that is expressed on endothelial cel ls (ECs) overlying human and rabbit advanced atherosclerotic plaques. The p resent study was designed to determine the temporal and spatial expression of IG9 and the chemokine, monocyte chemoattractant protein-1 (MCP-L), after balloon injury with (double injury) or without (single injury) prior air d esiccation EC injury in the femoral arteries of rabbits fed a high-choleste rol diet. By immunohistochemical analyses, intense reactivity with monoclon al antibodies to IG9 and MCP-1 was detected 24 hours after single injury in medial smooth muscle cells (SMCs) and in SMCs of adventitial microvessels, However, monocyte infiltration of the tunica media was minimal or not dete cted in these sections. IG9 and MCP-1 antibody reactivity in vessel section s 28 days after single injury and 24 hours, 7 days, and 28 days after doubl e injury was localized to medial and neointimal SMCs, foam cells, and lumin al ECs overlying the plaques. Uninjured rabbit (cholesterol or normal diet) vessel sections exhibited minimal IG9 and MCP-1 immunostaining. In vitro s tudies using human aortic SMCs demonstrated IG9 protein induction after 24 hours of treatment with platelet-derived growth factor-BE and interferon-ga mma or epidermal growth factor. IG9 expression was further increased by pre treatment of SMCs with the proatherogenic lipid, minimally oxidized low den sity lipoprotein. After balloon injury (24 hours), IG9 is induced in vascul ar SMCs before the detectable accumulation of monocytes within the vessel w all. Thus, the expression of IG9 by SMCs as well as by ECs may be an import ant factor in the accumulation of foam cells in atherosclerotic plaque deve lopment after arterial injury.