PMID- 10807745 OWN - NLM STAT- MEDLINE DCOM- 20000620 LR - 20190831 IS - 1079-5642 (Print) IS - 1079-5642 (Linking) VI - 20 IP - 5 DP - 2000 May TI - Induction of IG9 monocyte adhesion molecule expression in smooth muscle and endothelial cells after balloon arterial injury in cholesterol-fed rabbits. PG - 1293-300 AB - The expression of monocyte-specific adhesion molecules and chemokines by cell types within the vessel wall plays an important role in foam cell accumulation during atherosclerotic plaque development. We previously identified IG9, a novel monocyte adhesion protein that is expressed on endothelial cells (ECs) overlying human and rabbit advanced atherosclerotic plaques. The present study was designed to determine the temporal and spatial expression of IG9 and the chemokine, monocyte chemoattractant protein-1 (MCP-1), after balloon injury with (double injury) or without (single injury) prior air desiccation EC injury in the femoral arteries of rabbits fed a high-cholesterol diet. By immunohistochemical analyses, intense reactivity with monoclonal 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 detected in these sections. IG9 and MCP-1 antibody reactivity in vessel sections 28 days after single injury and 24 hours, 7 days, and 28 days after double injury was localized to medial and neointimal SMCs, foam cells, and luminal ECs overlying the plaques. Uninjured rabbit (cholesterol or normal diet) vessel sections exhibited minimal IG9 and MCP-1 immunostaining. In vitro studies using human aortic SMCs demonstrated IG9 protein induction after 24 hours of treatment with platelet-derived growth factor-BB and interferon-gamma or epidermal growth factor. IG9 expression was further increased by pretreatment of SMCs with the proatherogenic lipid, minimally oxidized low density lipoprotein. After balloon injury (24 hours), IG9 is induced in vascular SMCs before the detectable accumulation of monocytes within the vessel wall. Thus, the expression of IG9 by SMCs as well as by ECs may be an important factor in the accumulation of foam cells in atherosclerotic plaque development after arterial injury. FAU - Calderon, T M AU - Calderon TM AD - Department of Pathology, Albert Einstein College of Medicine, Bronx, NY, USA. calderon@aecom.yu.edu FAU - Gertz, S D AU - Gertz SD FAU - Sarembock, I J AU - Sarembock IJ FAU - Berliner, J A AU - Berliner JA FAU - Fallon, J T AU - Fallon JT FAU - Taubman, M B AU - Taubman MB FAU - Berman, J W AU - Berman JW LA - eng GR - HL-30568/HL/NHLBI NIH HHS/United States GR - HL-43302/HL/NHLBI NIH HHS/United States GR - HL-54469/HL/NHLBI NIH HHS/United States PT - Journal Article PT - Research Support, Non-U.S. Gov't PT - Research Support, U.S. Gov't, P.H.S. PL - United States TA - Arterioscler Thromb Vasc Biol JT - Arteriosclerosis, thrombosis, and vascular biology JID - 9505803 RN - 0 (Cell Adhesion Molecules) RN - 0 (Chemokine CCL2) RN - 0 (Cholesterol, Dietary) RN - 0 (Cytokines) RN - 0 (Growth Substances) RN - 0 (IG9 protein, Oryctolagus cuniculus) RN - 0 (Lipoproteins, LDL) RN - 0 (oxidized low density lipoprotein) SB - IM MH - Animals MH - Aorta MH - Carotid Artery Injuries/etiology/*metabolism MH - Catheterization MH - Cell Adhesion MH - Cell Adhesion Molecules/*genetics MH - Cells, Cultured MH - Chemokine CCL2/genetics MH - Cholesterol, Dietary/*administration & dosage MH - Cytokines/pharmacology MH - Endothelium, Vascular/*metabolism MH - *Gene Expression Regulation/drug effects MH - Growth Substances/pharmacology MH - Humans MH - Lipoproteins, LDL/pharmacology MH - Monocytes MH - Muscle, Smooth, Vascular/*metabolism MH - Rabbits EDAT- 2000/05/16 09:00 MHDA- 2000/06/24 11:00 CRDT- 2000/05/16 09:00 PHST- 2000/05/16 09:00 [pubmed] PHST- 2000/06/24 11:00 [medline] PHST- 2000/05/16 09:00 [entrez] AID - 10.1161/01.atv.20.5.1293 [doi] PST - ppublish SO - Arterioscler Thromb Vasc Biol. 2000 May;20(5):1293-300. doi: 10.1161/01.atv.20.5.1293.