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<csml:comment type="text">PMID: 9261091
There the LDL can undergo oxidative modification catalyzed by any of the major cell types found in arterial lesions, i.e. endothelial cells, smooth muscle cells, or macrophages.

PMID: 9261091,6587396
As mentioned above, modification of LDL by endothelial cells in vitro can be completely prevented by the addition of antioxidants such as vitamin E or butylated hydroxytoluene

PMID: 9261091, 8195716,9013599
Which of these contribute to LDL oxidation in vivo and to what extent is still uncertain, but analysis of products isolated from atherosclerotic lesions strongly supports the involvement of lipoxygenases and of myeloperoxidase

PMID: 9261091,9054771
Indeed this has now been demonstrated in several different animal models (the LDL receptor-deficient rabbit, the cholesterol-fed New Zealand White rabbit, the cholesterol-fed hamster, the cholesterol-fed cynomolgus monkey, the LDL receptor-deficient mouse, and the apoprotein E-deficient mouse) and using one of several different antioxidants (probucol, butylated hydroxytoluene, diphenylphenylenediamine, and vitamin E)</csml:comment>
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<csml:comment type="text">PMID: 9261091,1695010
Even minimally oxidized LDL (MM-LDL) can increase adherence and penetration of monocytes, in part by stimulating release of MCP-1 from endothelial cells</csml:comment>
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MM-LDL can also stimulate release of MCSF, which can induce differentiation of the monocyte into a cell with the phenotypic pattern of the tissue macrophage, including an increase in expression of SRA</csml:comment>
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MM-LDL can also stimulate release of MCSF, which can induce differentiation of the monocyte into a cell with the phenotypic pattern of the tissue macrophage, including an increase in expression of SRA

PMID: 9261091
More fully oxidized LDL (OxLDL) is itself directly chemotactic for monocytes, and it is also, of course, one of the major ligands for SRA and other receptors on the arterial macrophage that contribute to foam cell formation.</csml:comment>
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More fully oxidized LDL (OxLDL) is itself directly chemotactic for monocytes, and it is also, of course, one of the major ligands for SRA and other receptors on the arterial macrophage that contribute to foam cell formation.

PMID: 9261091,6301324
As already mentioned, the first property of oxidized LDL to be discovered that makes it more atherogenic than native LDL is that it is recognized by the scavenger receptors and can therefore give rise to foam cells </csml:comment>
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There the LDL can undergo oxidative modification catalyzed by any of the major cell types found in arterial lesions, i.e. endothelial cells, smooth muscle cells, or macrophages.

PMID: 9261091,6587396
As mentioned above, modification of LDL by endothelial cells in vitro can be completely prevented by the addition of antioxidants such as vitamin E or butylated hydroxytoluene

PMID: 9261091,8195716,9013599
Which of these contribute to LDL oxidation in vivo and to what extent is still uncertain, but analysis of products isolated from atherosclerotic lesions strongly supports the involvement of lipoxygenases and of myeloperoxidase

PMID: 9261091,9054771
Indeed this has now been demonstrated in several different animal models (the LDL receptor-deficient rabbit, the cholesterol-fed New Zealand White rabbit, the cholesterol-fed hamster, the cholesterol-fed cynomolgus monkey, the LDL receptor-deficient mouse, and the apoprotein E-deficient mouse) and using one of several different antioxidants (probucol, butylated hydroxytoluene, diphenylphenylenediamine, and vitamin E)</csml:comment>
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In fact the first antioxidant tested, probucol, does indeed have additional biological properties that might be relevant , including the ability to inhibit interleukin-1 release and to increase expression of cholesterol ester transfer protein. </csml:comment>
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In fact the first antioxidant tested, probucol, does indeed have additional biological properties that might be relevant , including the ability to inhibit interleukin-1 release and to increase expression of cholesterol ester transfer protein. </csml:comment>
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The B class of scavenger receptors includes CD36 and SR-B1

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<csml:comment type="text">PMID: 9261091,7685021,7520436
The B class of scavenger receptors includes CD36 and SR-B1

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Recent studies have shown that macrosialin and its human homologue, CD68, can bind OxLDL in ligand blots and that antibodies against CD68 can partially inhibit the binding and uptake of OxLDL by a human monocyte-derived cell line, the THP-1 cell line</csml:comment>
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The role of CD36 in this respect has been extensively studied (63) and appears to involve cooperative interaction with alpha Vbeta 3 and thrombospondin. </csml:comment>
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