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dc.contributor.advisorZhang, Cuihuaeng
dc.contributor.advisorDellsperger, Kevin C.eng
dc.contributor.authorMcAfee, Steven Rayeng
dc.date.issued2012eng
dc.date.submitted2012 Springeng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on September 13, 2012).eng
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.eng
dc.descriptionThesis advisors: Cuihua Zhang, Kevin C. Dellspergereng
dc.descriptionIncludes bibliographical references.eng
dc.descriptionVita.eng
dc.descriptionM.S. University of Missouri-Columbia 2012.eng
dc.descriptionDissertations, Academic -- University of Missouri--Columbia -- physiology (Medicine).eng
dc.description"May 2012"eng
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.eng
dc.format.extentv, 61 pageseng
dc.identifier.otherMcAfeeS-050712-T2199eng
dc.identifier.urihttp://hdl.handle.net/10355/15293eng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartof2012 Freely available theses (MU)eng
dc.relation.ispartofcommunityUniversity of Missouri-Columbia. Graduate School. Theses and Dissertations. Theses. 2012 Theseseng
dc.subjectatherosclerosiseng
dc.subjectendothelial functioneng
dc.subjectsoluble Receptor for Advanced Glycation (sRAGE)eng
dc.titleReceptor for advanced glycation end-products blockade improves endothelial dependent vascular function in atherosclerotic miceeng
dc.typeThesiseng
thesis.degree.disciplinePhysiology (Medicine) (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelMasterseng
thesis.degree.nameM.S.eng


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