Inhibition of Rupture of Established Atherosclerotic Plaques by Treatment with Apolipoprotein A-I

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dc.contributor.author Reimers, Gerrit en_US
dc.contributor.author Jackson, Christopher en_US
dc.contributor.author Rickards, Jasmine en_US
dc.contributor.author Chan, Peter en_US
dc.contributor.author Cohn, Jeffrey en_US
dc.contributor.author Rye, Kerry-Anne en_US
dc.contributor.author Barter, Philip en_US
dc.contributor.author Rodgers, Kenneth en_US
dc.contributor.editor en_US
dc.date.accessioned 2012-10-12T03:34:25Z
dc.date.available 2012-10-12T03:34:25Z
dc.date.issued 2011 en_US
dc.identifier 2011000544 en_US
dc.identifier.citation Reimers Gerrit et al. 2011, 'Inhibition of Rupture of Established Atherosclerotic Plaques by Treatment with Apolipoprotein A-I', Oxford Journals, vol. 91, no. 1, pp. 37-44. en_US
dc.identifier.issn 0008-6363 en_US
dc.identifier.other C1UNSUBMIT en_US
dc.identifier.uri http://hdl.handle.net/10453/18611
dc.description.abstract Aims Plasma concentrations of high-density lipoprotein (HDL)-cholesterol correlate inversely with the incidence of myocardial infarction in humans. We investigated the effect of treatment with human apolipoprotein A-I (apoA-I), the principal protein of HDL, on plaque disruption in an animal model. Methods and results Seventy apolipoprotein E knockout mice were induced to develop atherosclerotic lesions in the brachiocephalic artery by feeding a high-fat diet for 9 weeks. Mice then received twice-weekly treatment with human apoA-I (8 mg/kg) or vehicle, for 2 weeks. The incidence of acute plaque disruption was reduced by 65% in mice receiving apoA-I (P < 0.01). Plaques in treated mice had a more stable phenotype, with an increase in smooth muscle cell (SMC): macrophage ratio (P = 0.05), principally the consequence of an increase in the number of SMC in plaques. In the fibrous cap, there were reductions in matrix metalloproteinase-13 (-69%, P < 0.0001) and S100A4, a marker of SMC de-differentiation (-60%, P < 0.0001). These results indicate that 2 weeks of treatment with small amounts of human apoA-I produces more stable plaques in a mouse model. en_US
dc.language en_US
dc.publisher Oxford Journals en_US
dc.relation.isbasedon http://dx.doi.org/10.1093/cvr/cvr057 en_US
dc.title Inhibition of Rupture of Established Atherosclerotic Plaques by Treatment with Apolipoprotein A-I en_US
dc.parent Cardiovascular Research en_US
dc.journal.volume 91 en_US
dc.journal.number 1 en_US
dc.publocation United Kingdom en_US
dc.identifier.startpage 37 en_US
dc.identifier.endpage 44 en_US
dc.cauo.name SCI.Medical and Molecular Biosciences en_US
dc.conference Verified OK en_US
dc.for 110200 en_US
dc.personcode 0000076369 en_US
dc.personcode 0000076370 en_US
dc.personcode 0000076371 en_US
dc.personcode 0000076372 en_US
dc.personcode 0000076373 en_US
dc.personcode 0000066629 en_US
dc.personcode 0000066628 en_US
dc.personcode 111642 en_US
dc.percentage 100 en_US
dc.classification.name Cardiovascular Medicine and Haematology en_US
dc.classification.type FOR-08 en_US
dc.edition en_US
dc.custom en_US
dc.date.activity en_US
dc.location.activity en_US
dc.description.keywords Apolipoprotein A-I Plaque rupture, atherosclerosis, smooth muscle cells en_US
dc.staffid 111642 en_US


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