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dc.contributor.advisorZhang, Cuihuaen_US
dc.contributor.advisorDellsperger, Kevin C.en_US
dc.contributor.authorMcAfee, Steven Ray
dc.date.issued2012
dc.date.submitted2012 Springen_US
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on September 13, 2012).en_US
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.en_US
dc.descriptionThesis advisors: Cuihua Zhang, Kevin C. Dellspergeren_US
dc.descriptionIncludes bibliographical references.en_US
dc.descriptionVita.en_US
dc.descriptionM.S. University of Missouri-Columbia 2012.en_US
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- physiology (Medicine).en_US
dc.description"May 2012"en_US
dc.description.abstractAtherosclerosis is a progressive inflammatory disease that is present in large vessels in the body. We hypothesized that either adiponectin treatment or soluble Receptor for Advanced Glycation Products (sRAGE) treatment would rescue the decreased endothelial function of aortae in apolipoprotein-E knockout (ApoE-/-) mice, a murine model of atherosclerosis. We examined endothelialdependent vasorelaxation to acetylcholine (ACh) in aortae removed from ApoE-/- and control wild (WT) mice. Relaxation to ACh was blunted in ApoE-/- compared with WT controls while endothelial-independent vasorelaxation to sodium nitroprusside (SNP) was comparable. sRAGE improved ACh-induced vasorelaxation in ApoE-/- mice without affecting dilator response to SNP. Adiponectin treatment did not show significant improvement of endothelial function in aortae of ApoE-/- mice. Dilation to ACh was significantly attenuated after administration of nitric oxide (NO) synthase inhibitor NG-monomethyl Larginine in WT mice, which indicates that vasodilation to ACh was NO mediated while L-NMMA did not further inhibit endothelial-dependent vasodilation in ApoE-/- mice. Immunostaining showed RAGE to co-localized with the endothelium in murine aortae. These results suggest that AGE/RAGE signaling may play a pivotal role in processes that lead to endothelial dysfunction in atherosclerosis.en_US
dc.format.extentv, 61 pagesen_US
dc.identifier.otherMcAfeeS-050712-T2199
dc.identifier.urihttp://hdl.handle.net/10355/15293
dc.publisherUniversity of Missouri--Columbiaen_US
dc.relation.ispartof2012 Freely available theses (MU)en_US
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Theses. 2012 Theses
dc.subjectatherosclerosisen_US
dc.subjectendothelial functionen_US
dc.subjectsoluble Receptor for Advanced Glycation (sRAGE)en_US
dc.titleReceptor for advanced glycation end-products blockade improves endothelial dependent vascular function in atherosclerotic miceen_US
dc.typeThesisen_US
thesis.degree.disciplinePhysiology (Medicine)en_US
thesis.degree.disciplinePhysiology (Medicine)eng
thesis.degree.grantorUniversity of Missouri--Columbiaen_US
thesis.degree.levelMastersen_US
thesis.degree.nameM.S.en_US


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