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Titolo:
A common phenotype associated with atherogenesis in diverse mouse models of vascular lipid lesions
Autore:
Reckless, J; Rubin, EM; Verstuyft, JB; Metcalfe, JC; Grainger, DJ;
Indirizzi:
Univ Cambridge, Addenbrookes Hosp, Dept Med, Cambridge CB2 2QQ, England Univ Cambridge Cambridge England CB2 2QQ Med, Cambridge CB2 2QQ, England Univ Cambridge, Dept Biochem, Cambridge CB2 1QW, England Univ Cambridge Cambridge England CB2 1QW hem, Cambridge CB2 1QW, England Univ Calif Berkeley, Lawrence Berkeley Lab, Div Life Sci, Berkeley, CA 94720 USA Univ Calif Berkeley Berkeley CA USA 94720 ife Sci, Berkeley, CA 94720 USA
Titolo Testata:
JOURNAL OF VASCULAR RESEARCH
fascicolo: 3, volume: 38, anno: 2001,
pagine: 256 - 265
SICI:
1018-1172(200105/06)38:3<256:ACPAWA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; PLASMINOGEN-ACTIVATOR INHIBITOR; SMOOTH-MUSCLE CELLS; APOLIPOPROTEIN-A-I; TRANSGENIC MICE; TGF-BETA; ENDOTHELIAL-CELLS; ATHEROSCLEROTIC PLAQUES; ADJUVANT TAMOXIFEN; EXPRESSION;
Keywords:
arteries; atherosclerosis; macrophages; quantitative immunofluorescence; cytokines;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Reckless, J Univ Cambridge, Addenbrookes Hosp, Dept Med, Box 157,Hills Rd,Cambridge CB2 2QQ, England Univ Cambridge Box 157,Hills Rd Cambridge England CB2 2QQ and
Citazione:
J. Reckless et al., "A common phenotype associated with atherogenesis in diverse mouse models of vascular lipid lesions", J VASC RES, 38(3), 2001, pp. 256-265

Abstract

The introduction of a range of different genetic modifications in mice results in altered lipoprotein metabolism and the development of vascular lipid lesions. At present, however, it is unclear to what extent the molecular events underlying lipid lesion formation are similar in these different mouse models of atherosclerosis. The aim of this study was to compare the protein expression pattern of lipid lesions from seven different mouse lines with varying susceptibility to vascular lipid lesion development, to determine to what extent lesions induced by different genetic interventions have a similar composition. The proteins we have measured, using quantitative immunofluorescence, are proteins whose expression is known to be modulated during atherogenesis in humans, including plasminogen activator inhibitor (PAI)-1, transforming growth factor (TGF)-beta1, osteopontin and the macrophage marker CD11b. In all the mice lines we have investigated, PAI-1 was elevated wherever lesions developed. Active TGF-beta was depressed in the vessel wall of mice which developed lipid lesions, particularly in the intima. In contrast, TGF-beta1 antigen (active plus latent TGF-beta1) was increased at lesion sites. Accumulation of osteopontin and, with the marked exception ofapolipoprotein(a) transgenic mice, tissue macrophages occurred at sites oflipid deposition in the vessel wall. Each lesion, irrespective of its sizeand the mouse strain in which it developed, had similar amounts of PAI-1, active TGF-P and osteopontin per unit area of lesion. These data are consistent with a common phenotype accompanying atherogenesis, irrespective of the genetic basis of susceptibility. Copyright (C) 2001 S. Karger AG. Basel.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/03/20 alle ore 14:04:18