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Titolo:
Expression of mouse acute-phase (SAA1.1) and constitutive (SAA4) serum amyloid A isotypes - Influence on lipoprotein profiles
Autore:
Kindy, MS; de Beer, MC; Yu, J; de Beer, FC;
Indirizzi:
Univ Kentucky, Sch Med, Dept Biochem, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 ept Biochem, Lexington, KY 40536 USA Univ Kentucky, Sch Med, Dept Surg, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 , Dept Surg, Lexington, KY 40536 USA Univ Kentucky, Sch Med, Dept Internal Med, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 nternal Med, Lexington, KY 40536 USA Univ Kentucky, Sch Med, Sanders Brown Ctr Aging, Stroke Program, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 oke Program, Lexington, KY 40536 USA Dept Vet Affairs Med Ctr, Lexington, KY USA Dept Vet Affairs Med Ctr Lexington KY USA irs Med Ctr, Lexington, KY USA
Titolo Testata:
ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY
fascicolo: 6, volume: 20, anno: 2000,
pagine: 1543 - 1550
SICI:
1079-5642(200006)20:6<1543:EOMA(A>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
A GENE FAMILY; TRANSGENIC MICE; PHOSPHOLIPASE A(2); APOLIPOPROTEIN-E; DEFICIENT MICE; PROTEIN; DENSITY; SUBFRACTIONS; CHOLESTEROL; INDUCTION;
Keywords:
amyloidosis; atherosclerosis; inflammation; apolipoproteins; adenoviruses;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Kindy, MS Univ Kentucky, Med Ctr, Dept Biochem, 800 Rose St, Lexington, KY40536 USA Univ Kentucky 800 Rose St Lexington KY USA 40536 n, KY 40536 USA
Citazione:
M.S. Kindy et al., "Expression of mouse acute-phase (SAA1.1) and constitutive (SAA4) serum amyloid A isotypes - Influence on lipoprotein profiles", ART THROM V, 20(6), 2000, pp. 1543-1550

Abstract

The serum amyloid A (SAA) family of proteins consists of inducible acute-phase members and a constitutive member that are minor apolipoproteins of normal high density lipoprotein (HDL). During inflammation, HDL cholesterol and alaolipoprotein A-I (apoA-I) protein are decreased, and these changes are thought to be partly related to the increase in acute-phase SAA proteins that associate with the HDL particle to become the major apolipoprotein species. To determine the specific role of SAA. in the alteration of HDL in the absence of a generalized acute-phase response, acute-phase Saa1.1 transgene expression was directed via an inducible mouse metallothionein promoter. Elevated levels of SAA1.1 (28+/-9 mg/dL) comparable to a moderate acute-phase response were achieved over a 5-day period. SAA association with the HDL particles at this concentration did not significantly alter the apoA-I orHDL cholesterol levels or change the lipoprotein profiles in the transgenic mice compared with wild-type mice, In addition, we used adenoviral vectors to increase the SAA expression to levels seen in a major acute-phase response. Injection of adenovirus expressing the mouse SAA1.1 protein resulted in high-level expression (72+/-8 mg/dL) but did not alter apoA-I levels. However, the SAA associated with the HDL particle gave rise to significantly larger HDL particles ( approximate to 10%). Adenoviral expression of the constitutive SAA4 protein resulted in an increase in HDL size (approximate to10%) and an increase in very low density ligoprotein levels (20-fold) and triglyceride levels (1.7-fold), These studies suggest that increases in acute-phase SAA proteins alone are insufficient to alter HDL cholesterol or apoA-I levels during inflammation. A role for constitutive SAA4 in HDL-very low density lipoprotein interactions should be considered.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 22:18:34