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Titolo:
Increased atherosclerosis in LDL receptor-null mice lacking ACAT1 in macrophages
Autore:
Fazio, S; Major, AS; Swift, LL; Gleaves, LA; Accad, M; Linton, MF; Farese, RV;
Indirizzi:
Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Dept Med, Nashville, TN 37232 USA Vanderbilt Univ, Med Ctr, Dept Pathol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 pt Pathol, Nashville, TN 37232 USA Univ Calif San Francisco, Gladstone Inst Cardiovasc Dis, San Francisco, CA94143 USA Univ Calif San Francisco San Francisco CA USA 94143 rancisco, CA94143 USA Univ Calif San Francisco, Dept Med, San Francisco, CA 94143 USA Univ CalifSan Francisco San Francisco CA USA 94143 ancisco, CA 94143 USA Vanderbilt Univ, Med Ctr, Dept Pharmacol, Nashville, TN 37232 USA Vanderbilt Univ Nashville TN USA 37232 Pharmacol, Nashville, TN 37232 USA
Titolo Testata:
JOURNAL OF CLINICAL INVESTIGATION
fascicolo: 2, volume: 107, anno: 2001,
pagine: 163 - 171
SICI:
0021-9738(200101)107:2<163:IAILRM>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACYL-COENZYME-A; COA-CHOLESTEROL ACYLTRANSFERASE; E-DEFICIENT MICE; APOLIPOPROTEIN-E; ANTIATHEROSCLEROTIC AGENTS; MOLECULAR-CLONING; TRANSGENIC MICE; FOAM CELLS; IN-VIVO; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Fazio, S Vanderbilt Univ, Med Ctr, Div Cardiovasc Med, Dept Med, 315 Med Res Bldg 2, Nashville, TN 37232 USA Vanderbilt Univ 315 Med Res Bldg 2 Nashville TN USA 37232 232 USA
Citazione:
S. Fazio et al., "Increased atherosclerosis in LDL receptor-null mice lacking ACAT1 in macrophages", J CLIN INV, 107(2), 2001, pp. 163-171

Abstract

During atherogenesis, circulating macrophages migrate into the subendothelial space, internalize cholesterol-rich lipoproteins, and become foam cellsby progressively accumulating cholesterol esters. The inhibition of macrophage acyl coenzyme A:cholesterol acyltransferase (ACAT), which catalyzes the formation of cholesterol esters, has been proposed as a strategy to reduce foam cell formation and to treat atherosclerosis, We show here, however, that hypercholesterolemic LDL receptor-deficient (LDLR-/-) mice reconstituted with ACAT1-deficient macrophages unexpectedly develop larger atherosclerotic lesions than control LDLR-/- mice. The ACAT1-deficient lesions have reduced macrophage immunostaining and more free cholesterol than control lesions. Our findings suggest that selective inhibition of ACAT1 in lesion macrophages in the setting of hyperlipidemia can lead to the accumulation of free cholesterol in the artery wall, and that this promotes, rather than inhibits, lesion development.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/11/20 alle ore 15:44:37