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Titolo:
Regulation of acyl-coenzyme A : cholesterol acyltransferase (ACAT) synthesis, degradation, and translocation by high-density lipoprotein(2) at a low concentration
Autore:
Li, L; Pownall, HJ;
Indirizzi:
Baylor Coll Med, Dept Med, Houston, TX 77030 USA Baylor Coll Med Houston TX USA 77030 Med, Dept Med, Houston, TX 77030 USA Methodist Hosp, Houston, TX 77030 USA Methodist Hosp Houston TX USA 77030Methodist Hosp, Houston, TX 77030 USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 12, volume: 20, anno: 2000,
pagine: 2636 - 2642
SICI:
1079-5642(200012)20:12<2636:ROAA:C>2.0.ZU;2-T
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA LEVELS; HAMSTER OVARY CELLS; BREFELDIN-A; PLASMA-MEMBRANE; INTRACELLULAR-TRANSPORT; RADIATION INACTIVATION; MOLECULAR-CLONING; O-ACYLTRANSFERASE; COA; MACROPHAGES;
Keywords:
macrophage; lipid metabolism; cholesteryl ester; vesicular transport; ACAT;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Pownall, HJ Baylor Coll Med, Dept Med, MS A-601,6565 Fannin St, Houston, TX 77030 USA Baylor Coll Med MS A-601,6565 Fannin St Houston TX USA 77030 A
Citazione:
L. Li e H.J. Pownall, "Regulation of acyl-coenzyme A : cholesterol acyltransferase (ACAT) synthesis, degradation, and translocation by high-density lipoprotein(2) at a low concentration", ART THROM V, 20(12), 2000, pp. 2636-2642

Abstract

Although plasma HDL2 cholesterol concentration stands in inverse relation to risk for atherosclerotic disease, little is known about the mechanism ofthe apparent cardioprotection. In mouse P388D1 macrophages, HDL2 at a low concentration (less than or equal to 40 mug/mL) inhibits macrophage acyl-coenzyme A:cholesterol acyltransferase (ACAT), the enzyme that catalyzes esterification of intracellular cholesterol. The effects of HDL2 on ACAT synthesis, degradation, and intracellular translocation were investigated in mouse P388D1 macrophages. HDL2 at a low concentration enhanced ACAT synthesis but not total ACAT mass. Immunocytochemical studies showed that in the absence of lipoproteins, ACAT associated primarily with the perinuclear region of the cell. The addition of HDL2, however, induced the transfer of ACAT to vesicular structures and the cell periphery adjacent to the plasma membrane. Subfractionation combined with immunoprecipitation complemented these observations and showed that HDL2 promoted the transfer of ACAT to the plasma membrane fraction. Brefeldin A, which inhibits vesicular protein transport from the endoplasmic reticulum to the Golgi compartment in mammalian cells,blocked ACAT translocation and partially restored ACAT activity. These results suggest that HDL2 is an initiating factor in a signal transduction pathway that leads to intracellular ACAT translocation and inactivation.

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Documento generato il 23/01/21 alle ore 02:49:14