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Titolo:
Modification of type IIIVLDL, their remnants, and VLDL from ApoE-knockout mice by p-hydroxyphenylacetaldehyde, a product of myeloperoxidase activity,causes marked cholesteryl ester accumulation in macrophages
Autore:
Whitman, SC; Hazen, SL; Miller, DB; Hegele, RA; Heinecke, JW; Huff, MW;
Indirizzi:
Univ Western Ontario, Robarts Res Inst, London, ON N6A 5K8, Canada Univ Western Ontario London ON Canada N6A 5K8 London, ON N6A 5K8, Canada Univ Western Ontario, Dept Biochem, London, ON N6A 5K8, Canada Univ Western Ontario London ON Canada N6A 5K8 London, ON N6A 5K8, Canada Univ Western Ontario, Dept Med, London, ON N6A 5K8, Canada Univ Western Ontario London ON Canada N6A 5K8 London, ON N6A 5K8, Canada Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 d, Dept Med, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Mol Biol & Pharmacol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 & Pharmacol, St Louis, MO 63110 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 5, volume: 19, anno: 1999,
pagine: 1238 - 1249
SICI:
1079-5642(199905)19:5<1238:MOTITR>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; TRIGLYCERIDE-RICH LIPOPROTEINS; HUMAN ATHEROSCLEROTIC LESIONS; MOUSE PERITONEAL-MACROPHAGES; HUMAN MONOCYTE MACROPHAGES; PEROXIDE-CHLORIDE SYSTEM; RECEPTOR-MEDIATED UPTAKE; L-TYROSINE OXIDATION; E-DEFICIENT MICE; APOLIPOPROTEIN-E;
Keywords:
foam cells; atherosclerosis; in vitro; lipoproteins; reactive aldehydes;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
89
Recensione:
Indirizzi per estratti:
Indirizzo: Huff, MW UnivN6Astern Ontario, Robarts Res Inst, Room 4-16,100 Perth Dr, London, ON Univ Western Ontario Room 4-16,100 Perth Dr London ON Canada N6A 5K8
Citazione:
S.C. Whitman et al., "Modification of type IIIVLDL, their remnants, and VLDL from ApoE-knockout mice by p-hydroxyphenylacetaldehyde, a product of myeloperoxidase activity,causes marked cholesteryl ester accumulation in macrophages", ART THROM V, 19(5), 1999, pp. 1238-1249

Abstract

Very low density lipoproteins (VLDLs) from apolipoprotein (apo) E2/E2 subjects with type III hyperlipoproteinemia, VLDL remnants, and VLDL from apoE-knockout (EKO);mice are taken up poorly by macrophages. The present study examined whether VLDL modification by the reactive aldehyde p-hydroxyphenylacetaldehyde (pHA) enhances cholesteryl ester (CE) accumulation by J774A.1 macrophages. pHA is the major product derived from the oxidation of L-tyrosine by myeloperoxidase and is a component of human atherosclerotic lesions. Incubation of 57744.1 cells with native type III VLDL, their remnants, and EKO-VLDL increased cellular CE by only 3-, 5-, and 5-fold, respectively, compared with controls. In striking contrast, cells exposed to VLDL modified by purified pHA (pHA-VLDL) exhibited marked increases in cellular CE of 38-, 47-, and 35-fold, respectively (P less than or equal to 0.0001). Additionof the lipoprotein lipase inhibitor tetrahydrolipstatin decreased cellularCE accumulation induced by the 3 pHA-modified VLDL preparations by 73%, 59%, and 73%, respectively. Addition of the acyl coenzyme A:cholesterol acyltransferase. inhibitor DuP 128 to cells incubated with the pHA-modified lipoproteins decreased cellular CE by 100%, 82%, and 95%, respectively, but hadno effect on cellular triglycerides. To examine whether the type A scavenger receptors (SR-As) mediated the uptake of pHA-VLDL, incubations were performed in the presence of polyinosine (poly I), a polynucleotide known to block binding to SR-As (types I and II), or in cells preincubated with interferon-gamma (IFN-gamma), a cytokine known to decrease expression of SR-A type I. Coincubation of pHA-VLDL with poly I reduced cellular CE by only 38%; 44%, and 49%, respectively, whereas coincubation with IFN-gamma reduced CE by only 18%, 27%, and 65%, respectively. In marked contrast to pHA-VLDL, both poly I and IFN-gamma inhibited, by >95%, CE accumulation induced by copper-oxidized VLDL. These results demonstrate a novel mechanism for the conversion of type III VLDLs, their remnants, and EKO-VLDL into atherogenic particles and suggest that macrophage uptake of pHA-VLDL (1) requires catalytically active lipoprotein lipase, (2) involves acyl coenzyme A:cholesterol acyltransferase-mediated cholesterol esterification, and (3) involves pathways distinct from the SR-A.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 15:37:17