Transcription levels of ICAM-1 and PECAM-1 adhesion molecules are increased in the heart of APO-E knock-out mice in comparison to wild-type (C57BL6)

Zibara, K.; McGregor, Brigitte; Postin, R.; McGregor, John L.

doi:10.1016/s1567-5688(01)80184-7

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“…Moore versus ApoE −/− mice with a C57BL6 background. Immunohistochemical and transcriptomic results show that endothelial cell adhesion molecules in ApoE mice significantly change their expression as the plaque matures from a fibro fatty to a fibrotic state [55,56]. Such type of data can effectively be used to investigate the effects of CD36 deletion on vessel wall and plaque phenotype.…”

Section: Involvement Of Cd36 and Oxldl In Atherosclerotic Lesionsmentioning

confidence: 99%

CD36 and macrophages in atherosclerosis

Collot-Teixeira

Martin

McDermott-Roe

et al. 2007

Cardiovascular Research

330

256

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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

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Section: Involvement Of Cd36 and Oxldl In Atherosclerotic Lesionsmentioning

confidence: 99%