Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas
Autore:
Clubb, FJ; Cerny, JL; Deferrari, DA; Butler-Aucoin, MM; Willerson, JT; Buja, LM;
Indirizzi:
Texas Heart Inst, Dept Cardiovasc Pathol, Houston, TX 77225 USA Texas Heart Inst Houston TX USA 77225 ovasc Pathol, Houston, TX 77225 USA Univ Texas, Sch Med, Dept Internal Med, Houston, TX USA Univ Texas Houston TX USA s, Sch Med, Dept Internal Med, Houston, TX USA Univ Texas, Sch Med, Dept Pathol & Lab Med, Houston, TX USA Univ Texas Houston TX USA ch Med, Dept Pathol & Lab Med, Houston, TX USA
Titolo Testata:
CARDIOVASCULAR PATHOLOGY
fascicolo: 1, volume: 10, anno: 2001,
pagine: 1 - 11
SICI:
1054-8807(200101/02)10:1<1:DOAPWE>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
LOW-DENSITY-LIPOPROTEIN; CHOLESTEROL-FED RABBITS; FAT-FED RABBITS; FAMILIAL HYPERCHOLESTEROLEMIA; ANIMAL-MODEL; PLATELET-FUNCTION; WHHL-RABBIT; FISH-OIL; PROBUCOL; LESIONS;
Keywords:
Watanabe heritable hyperlipidemic rabbit; arteries; atherosclerosis; endothelial disruption; cholesterol; histopathology; macrophases; morphogenesis; immunostaining; transmission electron microscopy; scanning electron microscopy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Clubb, FJ Texas Heart Inst, Dept Cardiovasc Pathol, MC 1-283,POB 20345, Houston, TX 77225 USA Texas Heart Inst MC 1-283,POB 20345 Houston TX USA 77225 225 USA
Citazione:
F.J. Clubb et al., "Development of atherosclerotic plaque with endothelial disruption in Watanabe heritable hyperlipidemic rabbit aortas", CARDIO PATH, 10(1), 2001, pp. 1-11

Abstract

To better understand the morphogenesis of atherosclerotic plaque, we evaluated temporal distribution of leukocytes, macrophages, foam cells, vascularsmooth muscle cells, and subendothelial lipid in Watanabe heritable hyperlipedimic (WHHL) rabbit aortas. Aortas of WHHL (n = 20) and New Zealand White (NZW, controls; n = 8) rabbits were perfusion fixed at 1, 3, 6, and 12 months of age. At initial gross evaluation of lipid distribution, we identified aortic areas at high risk for lesion development. ln WHHL rabbits, the lipid-positive portion of high-risk areas increased from 3% at 1 month to 50% at 12 months; during the same period, adherent cell count increased from < 1 leukocyte and monocyte/mm(2) to 25 leukocytes, 44 monocytes, and 10 foam cells/mm(2). Controls showed no increase over time in lipid-positive areas or cellular adherence to the endothelium. One-month-old WHHL rabbit aortas had scattered lipid-positive cells in the intima (primarily branch points). Immunostaining of these areas did not show rabbit macrophages (RAM antibody) but were actin positive. Occasionally, platelets and monocytes adheredto the endothelial surface. By age 3 months, well-defined fatty streaks/atherosclerotic plaques had RAM-positive cells within foam cell core, along core margins, and in focal clusters in the fibrous cap and subendothelium. By age 12 months, isolated RAM-positive cells were on the endothelial surface, and surface morphology showed endothelial cell disruption foci containing clusters of macrophages and foam cells. Our results indicate that lipid accumulation (extra- and intracellular) is important in the early development of atherosclerotic lesions; a corresponding, slower accumulation of adherent cells on the lesion surface promotes lipid conversion from fatty streakto plaque. (C) 2001 Elsevier Science Inc. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 09:09:41