Please use this identifier to cite or link to this item: https://olympias.lib.uoi.gr/jspui/handle/123456789/9150
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dc.contributor.authorPapathanasiou, A. I.en
dc.contributor.authorLourida, E. S.en
dc.contributor.authorTsironis, L. D.en
dc.contributor.authorGoudevenos, J. A.en
dc.contributor.authorTselepis, A. D.en
dc.date.accessioned2015-11-24T16:47:12Z-
dc.date.available2015-11-24T16:47:12Z-
dc.identifier.issn0021-9150-
dc.identifier.urihttps://olympias.lib.uoi.gr/jspui/handle/123456789/9150-
dc.rightsDefault Licence-
dc.subjectoxidationen
dc.subjectatherosclerosisen
dc.subjectlipoproteinsen
dc.subjectatorvastainen
dc.subjectautoantibodiesen
dc.subjectlipoprotein-associated phospholipase a(2)en
dc.subjectpaf-acetylhydrolaseen
dc.subjectlow-density-lipoproteinen
dc.subjectactivating factor-acetylhydrolaseen
dc.subjectartery-diseaseen
dc.subjectpaf-acetylhydrolaseen
dc.subjectdegrading acetylhydrolaseen
dc.subjectoxidative modificationen
dc.subjectphospholipidsen
dc.subjecthypercholesterolemiaen
dc.subjectatherosclerosisen
dc.subjectantioxidantsen
dc.titleShort- and long-term elevation of autoantibody titers against oxidized LDL in patients with acute coronary syndromes - Role of the lipoprotein-associated phospholipase A(2) and the effect of atorvastatin treatmenten
heal.typejournalArticle-
heal.type.enJournal articleen
heal.type.elΆρθρο Περιοδικούel
heal.identifier.primaryDOI 10.1016/j.atherosclerosis.2006.10.033-
heal.identifier.secondary<Go to ISI>://000253341500037-
heal.identifier.secondaryhttp://ac.els-cdn.com/S0021915006006708/1-s2.0-S0021915006006708-main.pdf?_tid=906fa7d02083fe92597e539ce538a431&acdnat=1333111724_def0539fea8ea48a79b9a803c0d944bf-
heal.languageen-
heal.accesscampus-
heal.recordProviderΠανεπιστήμιο Ιωαννίνων. Σχολή Θετικών Επιστημών. Τμήμα Χημείαςel
heal.publicationDate2008-
heal.abstractOxidized low-density lipoprotein (oxLDL) is immunogenic while oxidized phospholipids (oxPL) formed on oxLDL and lysophosphatidylcholine (lyso-PC) generated during LDL oxidation through the hydrolysis of oxPL by the lipoprotein-associated phospholipase A(2) (Lp-PLA(2)), significantly contribute to oxLDL immunogenicity. We determined the autoantibody titers against various forms of mildly oxLDL in patients with acute coronary syndromes without persistent elevation of the ST segment (NSTE-ACS) and with undetectable serum levels of lipoprotein (a). Moreover, the effect of early atorvastatin administration on these autoantibody titers was evaluated. From the 133 consecutive NSTE-ACS patients, 55 were eligible for the study. Thirty-four received atorvastatin (group A), whereas 21 did not received any hypolipdemic therapy (group B). Two forms of copper-oxidized LDL were prepared at the end of propagation or decomposition phase (oxLDL(P) or oxLDL(D), respectively). Similar types of oxLDL were prepared after previous inactivation of the endogenous Lp-PLA(2) [oxLDL(-)]. In group B, autoantibody titers of IgG class against oxLDL(P) and oxLDL(D) were elevated at 1 month of follow-up to reach the baseline values 3 months afterwards. By contrast the titers against oxLDL(-)(P) and oxLDL(-)(D) increased at 1 month of follow-up and remained elevated for up to 6 months of follow-up. Atorvastatin treatment prevented the elevation of autoantibody titers against all forms of oxidized LDL. We conclude that a short-term immune response against oxLDL(P) and oxLDLD (enriched in lyso-PC) and a chronic immune response against oxLDL(-)(P) and oxLDL(-)(D) (enriched in oxPL) are observed after an NSTE-ACS, suggesting an important role of the LDL-associated Lp-PLA(2) in modulating these immune responses. Early atorvastatin treatment prevents both immune responses; however, the clinical significance of this effect remains to be established. (C) 2006 Elsevier Ireland Ltd. All rights reserved.en
heal.journalNameAtherosclerosisen
heal.journalTypepeer reviewed-
heal.fullTextAvailabilityTRUE-
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