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Titolo:
Increased cholesterol efflux in apolipoprotein AI (ApoAI)-producing macrophages as a mechanism for reduced atherosclerosis in ApoAI((-/-)) mice
Autore:
Major, AS; Dove, DE; Ishiguro, H; Su, YR; Brown, AM; Liu, L; Carter, KJ; Linton, MF; Fazio, S;
Indirizzi:
Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med,Sch Med, Nashville,TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 ed,Sch Med, Nashville,TN 37232 USA Vanderbilt Univ, Sch Med, Dept Pharmacol, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 Pharmacol, Nashville, TN 37212 USA Vanderbilt Univ, Sch Med, Dept Pathol, Nashville, TN 37212 USA Vanderbilt Univ Nashville TN USA 37212 pt Pathol, Nashville, TN 37212 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 11, volume: 21, anno: 2001,
pagine: 1790 - 1795
SICI:
1079-5642(200111)21:11<1790:ICEIAA>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIGH-DENSITY-LIPOPROTEIN; APOE-DEFICIENT MICE; BINDING CASSETTE TRANSPORTER-1; TANGIER-DISEASE; TRANSGENIC MICE; SCAVENGER RECEPTORS; LESION FORMATION; PLASMA-LEVELS; FOAM CELLS; EXPRESSION;
Keywords:
apoAI; transgenic mice; macrophage; foam cell;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Fazio, S Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med,Sch Med, 315 Med Res Bldg 2, Nashville, TN 37232 USA Vanderbilt Univ 315 Med Res Bldg2 Nashville TN USA 37232 232 USA
Citazione:
A.S. Major et al., "Increased cholesterol efflux in apolipoprotein AI (ApoAI)-producing macrophages as a mechanism for reduced atherosclerosis in ApoAI((-/-)) mice", ART THROM V, 21(11), 2001, pp. 1790-1795

Abstract

The concentration of apolipoprotein (apo) AI in the artery wall is thoughtto enhance cellular cholesterol efflux and protect against atherosclerosis. It has been shown that although macrophages do not make apoAI, they respond to it by increased cholesterol efflux. We hypothesized that macrophage production of apoAI would increase cholesterol efflux and reduce atherogenesis. In this study; we produced mice expressing human apoAI under the control of the macrophage-specific scavenger receptor-A promoter (mo-Al). Human apoAI was detectable in the serum HDL fraction of m phi -AI transgenic mice at concentrations too low to affect serum cholesterol or HDL levels. Immunoblotting showed the presence of human apoAI in transgenic macrophage culture supernatants, mostly as lipoprotein-free protein, with a small component associated with HDL-like particles. Atherosclerosis studies using apoAI((-/-)) mice transplanted with m phi -AI bone marrow showed that in the absenceof macrophage-derived apoE, local expression of apoAI reduced diet-inducedlesions in the proximal aorta. Additionally, m phi -AI macrophages showed a 40% increase in cholesterol efflux compared with control macrophages. These data support the hypothesis that apoAl production by macrophages in the artery wall is protective against atherosclerosis. This protection is likely mediated by increased cholesterol efflux and decreased foam cell formation in vivo.

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Documento generato il 04/12/20 alle ore 06:38:38