CD36 is a multi-ligand scavenger receptor present on the surface of a number of cells such as platelets, monocytes/macrophages, endothelial and smooth muscle cells. Monocyte/macrophage CD36 has been shown to play a critical role in the development of atherosclerotic lesions by its capacity to bind and endocytose oxidized low density lipoproteins (OxLDL), and it is implicated in the formation of foam cells. However, the significance of CD36 in atherosclerosis has recently been called into question by different studies, and therefore its exact role still needs to be clarified. The aim of this article is to carefully review the importance of CD36 as an essential component in the pathogenesis of atherosclerosis. © 2007 European Society of Cardiology. Published by Elsevier B.V. All rights reserved.Keywords: CD36; Vascular; Monocyte/macrophages; OxLDL; Atherosclerosis Atherosclerosis is a progressive chronic inflammatory disease characterised by a gradual thickening and hardening of arteries that ultimately leads to a reduction in the lumen diameter and potentially to ischemia following plaque rupture. A first stage of the disease is the presence of dysfunctional endothelial cells (EC) which via activated adhesion molecules and expressed chemokines recruit circulating monocytes and a subpopulation of lymphocytes (CD4/CD8) into the intima. Endothelial dysfunction may be induced by oxidized low density lipoproteins (OxLDL). Indeed, LDL when infiltrating into the intima can be readily oxidized by resident macrophages or endothelial cells. Moreover, C-reactive protein (CRP) and OxLDL can act synergistically to increase monocytes inflammatory properties (through MCP-1, PGE2, MMP-1 production) and attract further circulating monocytes through the release of MCP-1 to adhere to the activated dysfunctional endothelial cells and extravasate to the intima to scavenge OxLDL [1]. One of the involvements of CD36 in lesion development is its ability to bind and endocytose OxLDL into macrophages, as a scavenger receptor, and ultimately be implicated in the differentiation of resident macrophages into foam cells that constitute the atherosclerotic lesion core.CD36 is an 88-kD membrane glycoprotein that was first identified on monocytes by monoclonal antibody OKM5 [2] and then subsequently isolated from blood platelets [3,4]. This membrane glycoprotein is expressed by many celltypes including microvasculature endothelial [5] and smooth muscle cells (SMC) [6]. Functional and structural characterisation showed CD36 to be a member of the scavenger receptor class B family with a capacity to bind OxLDL as well as various other ligands. The importance of monocytic CD36 in the initiation and perpetuation of atherosclerotic lesions was shown over this past decade by its effect in significantly reducing the size of vascular lesions when

Objectives-To compare, by immunohistochemistry, the cellular and cytokine profile in rheumatoid arthritis

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Variation on chromosome 9p21 is associated with risk of coronary artery disease (CAD). This genomic region contains the CDKN2A and CDKN2B genes which encode the cell cycle regulators p16(INK4a), p14(ARF) and p15(INK4b) and the ANRIL gene which encodes a non-coding RNA. Vascular smooth muscle cell (VSMC) proliferation plays an important role in the pathogenesis of atherosclerosis which causes CAD. We ascertained whether 9p21 genotype had an influence on CDKN2A/CDKN2B/ANRIL expression levels in VSMCs, VSMC proliferation and VSMC content in atherosclerotic plaques. Immunohistochemical examination showed that VSMCs in atherosclerotic lesions expressed p16(INK4a), p14(ARF) and p15(INK4b). Analyses of primary cultures of VSMCs showed that the 9p21 risk genotype was associated with reduced expression of p16(INK4a), p15(INK4b) and ANRIL (P = 1.2 × 10(-5), 1.4 × 10(-2) and 3.1 × 10(-9)) and with increased VSMC proliferation (P = 1.6 × 10(-2)). Immunohistochemical analyses of atherosclerotic plaques revealed an association of the risk genotype with reduced p15(INK4b) levels in VSMCs (P = 3.7 × 10(-2)) and higher VSMC content (P = 5.6 × 10(-4)) in plaques. The results of this study indicate that the 9p21 variation has an impact on CDKN2A and CDKN2B expression in VSMCs and influences VMSC proliferation, which likely represents an important mechanism for the association between this genetic locus and susceptibility to CAD.