Modulation of Expression of Endothelial Intercellular Adhesion Molecule-1, Platelet–Endothelial Cell Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Aortic Arch Lesions of Apolipoprotein E–Deficient Compared With Wild-Type Mice

Zibara, Kazem; Chignier, E.; Covacho, C.; Poston, Robin N.; Canard, Georges; Hardy, Patrick; McGregor, John L.

doi:10.1161/01.atv.20.10.2288

Cited by 61 publications

(41 citation statements)

References 49 publications

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“…ApoE-enriched lipoproteins from diet-induced wild-type mice may be proatherogenic. Increased ICAM-1 and VCAM-1 expression has been suggested to be associated with or to predict atherosclerotic lesions (22)(23)(24). Reduced expression of these adhesion molecules has been shown to protect against atherosclerosis in mice (25,26).…”

Section: Discussionmentioning

confidence: 99%

“…Atherosclerosis is a chronic inflammatory disease in which early atherogenic events include increased expression of vascular adhesion molecules and chemoattractants, followed by increased adhesion of monocytes and lymphocytes (17). Increased intercellular adhesion molecule-1 (ICAM-1) and vascular cell adhesion molecule-1 (VCAM-1) expression has been shown to be associated with or to predict atherosclerosis (22)(23)(24). To assess the atherogenic potential of the diet-induced hyperlipidemic wild-type and PLTP-deficient mice, we analyzed the expression of proatherogenic VCAM-1 and ICAM-1 in aorta.…”

Section: Effects Of Pltp Deficiency On Aortic and Systemic Inflammationmentioning

confidence: 99%

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Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice

Shelly

Royer

Sand

et al. 2008

Journal of Lipid Research

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Phospholipid transfer protein (PLTP) facilitates the transfer of phospholipids from triglyceride-rich lipoproteins into HDL. PLTP has been shown to be an important factor in lipoprotein metabolism and atherogenesis. Here, we report that chronic high-fat, high-cholesterol diet feeding markedly increased plasma cholesterol levels in C57BL/6 mice. PLTP deficiency attenuated diet-induced hypercholesterolemia by dramatically reducing apolipoprotein E-rich lipoproteins (288%) and, to a lesser extent, LDL (240%) and HDL (235%). Increased biliary cholesterol secretion, indicated by increased hepatic ABCG5/ABCG8 gene expression, and decreased intestinal cholesterol absorption may contribute to the lower plasma cholesterol in PLTP-deficient mice. The expression of proinflammatory genes (intercellular adhesion molecule-1 and vascular cell adhesion molecule-1) is reduced in aorta of PLTP knockout mice compared with wild-type mice fed either a chow or a high-cholesterol diet. Furthermore, plasma interleukin-6 levels are significantly lower in PLTP-deficient mice, indicating reduced systemic inflammation. These data suggest that PLTP appears to play a proatherogenic role in dietinduced hyperlipidemic mice. Plasma phospholipid transfer protein (PLTP) plays an important role in the metabolism of lipoproteins (1). PLTP belongs to the family of lipid transfer/lipopolysaccharide binding proteins, including cholesteryl ester transfer protein, lipopolysaccharide binding protein, and bactericidal permeability-increasing protein (2, 3). It has been shown that PLTP facilitates the transfer and exchange of phospholipids between VLDL and HDL (4). It also transfers phospholipids between HDL particles that result in the conversion of HDL 3 into larger and smaller HDL particles (5, 6). PLTP can also bind several other amphipathic molecules, including a-tocopherol, diacylglycerides, cerebrosides, and lipopolysaccharides (7). Several clinical studies suggest that high plasma PLTP activity is a risk factor for coronary artery disease and a determinant of carotid intimamedia thickness in type 2 diabetes mellitus (8, 9).Studies using genetically modified mice strongly suggest that PLTP functions as a proatherogenic factor (10-12). PLTP deficiency causes a marked decrease in HDL lipids and apolipoprotein A-I (apoA-I), as a result of higher catabolism, in both chow-fed and 2 week Western diet-fed mice (13,14). The absence of PLTP in hyperlipidemic apoE-deficient and human apoB transgenic mouse strains results in reduced production in plasma levels of apoBcontaining lipoproteins, mostly LDL (10). Atherosclerotic lesion areas are also decreased in PLTP knockout mice in the LDL receptor-or apoE-deficient or apoB transgenic background, despite decreased HDL. Furthermore, reduced lipoprotein oxidation and improved anti-inflammatory properties of HDL in PLTP knockout mice may also contribute to the antiatherogenic potential in these mouse models (15,16). The proatherogenic role of PLTP is further supported by results that demonstrate increased ...

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Section: Discussionmentioning

confidence: 99%

Section: Effects Of Pltp Deficiency On Aortic and Systemic Inflammationmentioning

confidence: 99%

Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice

Shelly

Royer

Sand

et al. 2008

Journal of Lipid Research

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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

332

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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“…24 Similarly,an increased plasma level of soluble PECAM-1 has been reported in patients with cardiovascular disease 25,26 and in animal models of atherosclerosis such as the apolipoprotein E knockout mice. 27 Because PECAM-1 expression may be a prerequisite for VEGF-induced vasculogenesis and also angiogenesis, and because LacCer can upregulate PECAM-1 expression in U937 cells, we rationalized that LacCer may well play a second messenger role in VEGF-induced PECAM-1 expression and angiogenesis in human endothelial cells. In the present article, we describe how LacCer is critical in mediating VEGF-induced PECAM-1 expression and angiogenesis in human umbilical vein endothelial cells (HUVECs).…”

mentioning

confidence: 97%

Novel Role of Lactosylceramide in Vascular Endothelial Growth Factor–Mediated Angiogenesis in Human Endothelial Cells

Rajesh

Kolmakova

Chatterjee

2005

Circulation Research

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Abstract-Vascular endothelial growth factor (VEGF) has been implicated in angiogenesis associated with coronary heart disease, vascular complications in diabetes, inflammatory vascular diseases, and tumor metastasis. The mechanism of VEGF-driven angiogenesis involving glycosphingolipids such as lactosylceramide (LacCer), however, is not known. To demonstrate the involvement of LacCer in VEGF-induced angiogenesis, we used small interfering RNA (siRNA)-mediated silencing of LacCer synthase expression (GalT-V) in human umbilical vein endothelial cells. This gene silencing markedly inhibited VEGF-induced platelet endothelial cell adhesion molecule-1 (PECAM-1) expression and angiogenesis. Second, we used D-threo-1-phenyl-2-decanoylamino-3-morpholino-1-propanol (D-PDMP), an inhibitor of LacCer synthase and glucosylceramide synthase, that significantly mitigated VEGF-induced PECAM-1 expression and angiogenesis. Interestingly, these phenotypic changes were reversed by LacCer but not by structurally related compounds such as glucosylceramide, digalactosylceramide, and ceramide. In a human mesothelioma cell line (REN) that lacks the endogenous expression of PECAM-1, VEGF/LacCer failed to stimulate PECAM-1 expression and tube formation/angiogenesis. In REN cells expressing human PECAM-1 gene/protein, however, both VEGF and LacCerinduced PECAM-1 protein expression and tube formation /angiogenesis. In fact, VEGF-induced but not LacCerinduced angiogenesis was mitigated by SU-1498, a VEGF receptor tyrosine kinase inhibitor. Also, VEGF/LacCerinduced PECAM-1 expression and angiogenesis was mitigated by protein kinase C and phospholipase A 2 inhibitors. These results indicate that LacCer generated in VEGF-treated endothelial cells may serve as an important signaling molecule for PECAM-1 expression and in angiogenesis. This finding and the reagents developed in our report may be useful as anti-angiogenic drugs for further studies in vitro and in vivo. Key Words: vascular endothelial growth factor Ⅲ lactosylceramide Ⅲ platelet endothelial cell adhesion molecule-1 Ⅲ angiogenesis V ascular endothelial growth factor (VEGF) has been implicated in the process of vasculogenesis and angiogenesis. 1,2 Aberrant expression of VEGF has been reported in several vascular pathologies such as inflammation, complications of diabetes mellitus, cardiovascular diseases, and tumor metastasis. 3 VEGF binds to its receptors KDR/Flk-1 to mediate its effect on angiogenesis in physiological conditions and in human atherosclerosis. 4 -6 Platelet endothelial cell adhesion molecule-1 (PECAM-1)/ CD31 is a constitutively expressed integral protein in endothelial cells. 7 In addition, PECAM-1 is expressed in platelets, monocytes, neutrophils, and a certain subset of T cells. 8 Recent studies implicate PECAM-1 in angiogenesis and in vitro endothelial cell migration. 9,10 For example, human mesothelioma cell line (REN) that is deficient in PECAM-1 10 and cells from PECAM-1 deficient mice 11 did not form tubes in vitro (angiogenesis). In contrast, REN cells overe...

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Modulation of Expression of Endothelial Intercellular Adhesion Molecule-1, Platelet–Endothelial Cell Adhesion Molecule-1, and Vascular Cell Adhesion Molecule-1 in Aortic Arch Lesions of Apolipoprotein E–Deficient Compared With Wild-Type Mice

Cited by 61 publications

References 49 publications

Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice

Phospholipid transfer protein deficiency ameliorates diet-induced hypercholesterolemia and inflammation in mice

CD36 and macrophages in atherosclerosis

Novel Role of Lactosylceramide in Vascular Endothelial Growth Factor–Mediated Angiogenesis in Human Endothelial Cells

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