Please use this identifier to cite or link to this item: https://ahro.austin.org.au/austinjspui/handle/1/9411
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dc.contributor.authorCandido, Riccardoen
dc.contributor.authorJandeleit-Dahm, Karin Aen
dc.contributor.authorCao, Zeminen
dc.contributor.authorNesteroff, Stefan Pen
dc.contributor.authorBurns, Wendy Cen
dc.contributor.authorTwigg, Stephen Men
dc.contributor.authorDilley, Rodney Jen
dc.contributor.authorCooper, Mark Een
dc.contributor.authorAllen, Terri Jen
dc.date.accessioned2015-05-15T22:29:47Z
dc.date.available2015-05-15T22:29:47Z
dc.date.issued2002-07-09en
dc.identifier.citationCirculation; 106(2): 246-53en
dc.identifier.govdoc12105166en
dc.identifier.otherPUBMEDen
dc.identifier.urihttp://ahro.austin.org.au/austinjspui/handle/1/9411en
dc.description.abstractAtherosclerosis is a major complication of diabetes, but the mechanisms by which diabetes promotes macrovascular disease have not been fully delineated. Although several animal studies have demonstrated that inhibition of ACE results in a decrease in the development of atherosclerotic lesions, information about the potential benefits of these agents on complex and advanced atherosclerotic lesions as observed in long-term diabetes is lacking. The aim of this study was to evaluate whether treatment with the ACE inhibitor perindopril affects diabetes-induced plaque formation in the apolipoprotein E (apoE)-deficient mouse.Diabetes was induced by injection of streptozotocin in 6-week-old apoE-deficient mice. Diabetic animals received treatment with perindopril (4 mg x kg(-1) x d(-1)) or no treatment for 20 weeks. Nondiabetic apoE-deficient mice were used as controls. Induction of diabetes was associated with a 4-fold increase in plaque area compared with nondiabetic animals. This accelerated atherosclerosis was associated with a significant increase in aortic ACE expression and activity and connective tissue growth factor and vascular cell adhesion molecule-1 expression. Perindopril treatment inhibited the development of atherosclerotic lesions and diabetes-induced ACE, connective tissue growth factor, and vascular cell adhesion molecule-1 overexpression in the aorta.The activation of the local renin-angiotensin system in the diabetic aorta and the reduction in atherosclerosis with ACE inhibitor treatment provides further evidence that the renin-angiotensin system plays a pivotal role in the development and acceleration of atherosclerosis in diabetes.en
dc.language.isoenen
dc.subject.otherActins.analysisen
dc.subject.otherAngiotensin-Converting Enzyme Inhibitors.therapeutic useen
dc.subject.otherAnimalsen
dc.subject.otherAorta.chemistry.metabolism.pathologyen
dc.subject.otherApolipoproteins E.geneticsen
dc.subject.otherArteriosclerosis.etiology.metabolism.pathology.prevention & controlen
dc.subject.otherCollagen.analysisen
dc.subject.otherConnective Tissue Growth Factoren
dc.subject.otherDiabetes Mellitus, Experimental.complicationsen
dc.subject.otherDisease Progressionen
dc.subject.otherGrowth Substances.biosynthesis.geneticsen
dc.subject.otherImmediate-Early Proteins.biosynthesis.geneticsen
dc.subject.otherIntercellular Signaling Peptides and Proteinsen
dc.subject.otherMaleen
dc.subject.otherMiceen
dc.subject.otherMice, Inbred C57BLen
dc.subject.otherMice, Knockouten
dc.subject.otherMuscle, Smooth, Vascular.chemistryen
dc.subject.otherPeptidyl-Dipeptidase A.genetics.metabolismen
dc.subject.otherPerindopril.therapeutic useen
dc.subject.otherPhagocytes.physiologyen
dc.subject.otherProliferating Cell Nuclear Antigen.analysisen
dc.subject.otherRNA, Messenger.biosynthesisen
dc.subject.otherVascular Cell Adhesion Molecule-1.biosynthesis.geneticsen
dc.titlePrevention of accelerated atherosclerosis by angiotensin-converting enzyme inhibition in diabetic apolipoprotein E-deficient mice.en
dc.typeJournal Articleen
dc.identifier.journaltitleCirculationen
dc.identifier.affiliationDepartment of Medicine, University of Melbourne, Austin and Repatriation Medical Centre, Heidelberg West, Australiaen
dc.description.pages246-53en
dc.relation.urlhttps://pubmed.ncbi.nlm.nih.gov/12105166en
dc.type.austinJournal Articleen
item.fulltextNo Fulltext-
item.openairetypeJournal Article-
item.grantfulltextnone-
item.cerifentitytypePublications-
item.languageiso639-1en-
item.openairecristypehttp://purl.org/coar/resource_type/c_18cf-
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