Atherosclerosis and autoimmunity section V, Anti-endothelial by Yehuda Shoenfeld; Dror Harats; Georg Wick; et al

By Yehuda Shoenfeld; Dror Harats; Georg Wick; et al

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Haust MD. The natural history of human atherosclerotic lesions. , New York, 1981; 1-23. Mclyill HC, Geer JC, Stron JP. Natural history of human atherosclerotic lesions. In: Atherosclerosis and Its Origin, Sander M, Bourne GH, editors, Academic Press, New York, 1963;39-65. Rosenfeld ME, Ross R. Macrophage and smooth muscle cell proliferation in atheroscleroticlesion of WHHL and 14. 15. comparably hypercholesterolemic fat-fed rabbits. Arteriosclerosis 1990;10:680-687. Ruan Y, Takahashi K, Naito M.

Free cholesterol is released from the lysosomes into the cytosol, excess of cholesterol ester is accumulated in membrane-free lipid droplets by catalyzing with acyl coenzyme Axholesterol acyItransferase-1 (ACAT-1), and intracellular accumulation of lipid droplets changes macrophages into foam cells [6,7]. In the atherosclerotic plaques, the number of macrophage-derived foam cells increases more than in the fatty streak lesions, and besides the macrophagederived foam cells, smooth muscle cells migrate from the subintimal layer and media of arteries.

C: On day 7 after coculture with a mixture of OxLDL into a collagen gel layer, macrophages transform into foam cells by accumulating lipid droplets (M(|)). Original magnifications: A, x 3,000; B, x 3,500; C, x 1,500. phages in various organs and tissues [65-68]. In op/op mice, monocyte migration into inflammatory foci is severely impaired [66]. In mice deficient in both M-CSF {op) and apoE, the frequency of atherosclerosis development is severely reduced, demonstrating that M-CSF is important for atherogenesis [69-71].

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