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Titolo:
TGF-P reduced binding of high-density lipoproteins in murine macrophages and macrophage-derived foam cells
Autore:
Zuckerman, SH; Panousis, C; Evans, G;
Indirizzi:
Eli Lilly & Co, Lilly Res Lab, Div Cardiovasc Res, Indianapolis, IN 46285 USA Eli Lilly & Co Indianapolis IN USA 46285 Res, Indianapolis, IN 46285 USA
Titolo Testata:
ATHEROSCLEROSIS
fascicolo: 1, volume: 155, anno: 2001,
pagine: 79 - 85
SICI:
0021-9150(200103)155:1<79:TRBOHL>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
GROWTH-FACTOR-BETA; REVERSE CHOLESTEROL TRANSPORT; B TYPE-I; SCAVENGER RECEPTOR; GENE-EXPRESSION; ATHEROSCLEROTIC LESIONS; TARGETED MUTATION; INTERFERON-GAMMA; HUMAN CD36; SR-BI;
Keywords:
cytokines; lipoproteins; flow cytometry; scavenger receptors;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Zuckerman, SH Eli Lilly & Co, Lilly Res Lab, Div Cardiovasc Res, Indianapolis, IN 46285 USA Eli Lilly & Co Indianapolis IN USA 46285 olis, IN 46285 USA
Citazione:
S.H. Zuckerman et al., "TGF-P reduced binding of high-density lipoproteins in murine macrophages and macrophage-derived foam cells", ATHEROSCLER, 155(1), 2001, pp. 79-85

Abstract

The expression of macrophage scavenger receptors is regulated by intracellular cholesterol levels, as well as by cytokines affecting macrophage effector functions. CD36, a member of the type B scavenger receptor family, willbind a variety of nonlipoprotein and lipoprotein ligands including high-density lipoprotein (HDL). Transforming growth factor-beta (TGF-beta) has been demonstrated to modulate macrophage effector functions and is present within atherosclerotic lesions. In the present study, the effect of TGF-beta on HDL binding by both macrophages and macrophage-derived foam cells was evaluated. TGF-beta, in a dose-dependent manner, reduced the binding of flurochrome-labeled HDL to both macrophages and foam cells. These effects were observed in macrophages derived from nonatherosclerotic (BALB/c) as well as from macrophages obtained from both apolipoprotein E and low-density lipoprotein receptor knockout mice. The decrease in HDL binding was consistent with a significant reduction in CD36 message levels. The effect of TGF-beta ontype B scavenger receptor expression was not limited to CD36 as SR-BI message was also downregulated, although the effect was more modest. A similar reduction in HDL binding and CD36 message was also observed with the immunosuppressive glucocorticoid dexamethasone. These results suggest that withinthe microenvironment of an atherosclerotic lesion, TGF-beta and other agents that inhibit macrophage inflammatory responses may impact lesion progression through mechanisms that include the modulation of HDL-foam cell interactions. (C) 2001 Elsevier Science Ireland Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 02/10/20 alle ore 01:05:18