Accumulation of Cholesteryl Ester in Atherosclerotic Lesions

Amyloid fibrils are fibrillar polypeptide aggregates from several degenerative human conditions, including Alzheimer's and Creutzfeldt-Jakob diseases. Analysis of amyloid fibrils derived from various human diseases (AA, ATTR, A␤2M, AL , and AL amyloidosis) shows that these are associated with a common lipid component that has a conserved chemical composition and that is specifically rich in cholesterol and sphingolipids, the major components of cellular lipid rafts. This pattern is not notably affected by the purification procedure, and no tight lipid interactions can be detected when preformed fibrils are mixed with lipids. By contrast, the early and prefibrillar aggregates formed in an AA amyloidproducing cell system interact with the raft marker ganglioside-1, and amyloid formation is impaired by addition of cholesterolreducing agents. These data suggest the existence of common cellular mechanisms in the generation of different types of clinical amyloid deposits.protein folding ͉ prion ͉ lipid rafts

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Raft lipids as common components of human extracellular amyloid fibrils

Gellermann

Appel

Tannert

et al. 2005

Proc. Natl. Acad. Sci. U.S.A.

190

163

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Molecular Pathology in Atherosclerosis: The Mechanism How Cholesteryl Ester Accumulates in Atheromatous Aorta

et al. 2008

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To study how cholesterol accumulates in atheroma, novel monoclonal antibodies were developed, using crude homogenate of atheroma as immunogens. 212D monoclonal antibody recognizing extra cellular matrix with lipid-laden deposits was selected by histochemical staining. The antigen was deduced vitronectin from cDNA library. DLH3 monoclonal antibody recognizing oxidized LDL, epitope of which was 5-or 9-phosphatidylcholine. Signiˆcant correlations between oxidized LDL and coronary heart disease (CHD) patients were observed from clinical study. 256C monoclonal antibody recognizing atheromatous lesions in human aorta was selected. Epitope must be PC-cholesterol complex which may involve in foam cell rupture. Atherogenesis will be discussed from the aspects of these antibodies. Our working hypothesis is required to elucidate the mechanism. Denatured lipoproteins (either oxidized lipoprotein or ruptured foam cells) may induce atheroma. Oxidation of lipoprotein may be taken place both in foam cells and/or extra cellular matrix, and macrophage eliminate these denatured lipoproteins and become foam cells. The foam cells are ruptured by either apoptosis or necrosis afterward, and hydrophobic fragments of foam cells dispersed in extra cellular space, which destroys the function of biological membrane. Since biological function could be maintained by segregation of hydrophilic circumstances, macrophages uptake these fragmented material and oxidized lipoprotein to maintain the function. This vicious spiral may enhance chronically the atheroma.

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Accumulation of Cholesteryl Ester in Atherosclerotic Lesions

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References 12 publications

Raft lipids as common components of human extracellular amyloid fibrils

Raft lipids as common components of human extracellular amyloid fibrils

Molecular Pathology in Atherosclerosis: The Mechanism How Cholesteryl Ester Accumulates in Atheromatous Aorta

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