Receptor for advanced glycation end-products blockade improves endothelial dependent vascular function in atherosclerotic mice

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Receptor for advanced glycation end-products blockade improves endothelial dependent vascular function in atherosclerotic mice

Please use this identifier to cite or link to this item: http://hdl.handle.net/10355/15293

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dc.contributor.advisor Zhang, Cuihua en_US
dc.contributor.advisor Dellsperger, Kevin C. en_US
dc.contributor.author McAfee, Steven Ray
dc.date.accessioned 2012-09-13T19:25:40Z
dc.date.available 2012-09-13T19:25:40Z
dc.date.issued 2012
dc.date.submitted 2012 Spring en_US
dc.identifier.other McAfeeS-050712-T2199
dc.identifier.uri http://hdl.handle.net/10355/15293
dc.description Title from PDF of title page (University of Missouri--Columbia, viewed on September 13, 2012). en_US
dc.description The 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.description Thesis advisors: Cuihua Zhang, Kevin C. Dellsperger en_US
dc.description Includes bibliographical references. en_US
dc.description Vita. en_US
dc.description M.S. University of Missouri-Columbia 2012. en_US
dc.description Dissertations, Academic -- University of Missouri--Columbia -- physiology (Medicine). en_US
dc.description "May 2012" en_US
dc.description.abstract Atherosclerosis 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.extent v, 61 pages en_US
dc.language.iso en_US en_US
dc.publisher University of Missouri--Columbia en_US
dc.relation.ispartof 2012 Freely available theses (MU) en_US
dc.subject atherosclerosis en_US
dc.subject endothelial function en_US
dc.subject soluble Receptor for Advanced Glycation (sRAGE) en_US
dc.title Receptor for advanced glycation end-products blockade improves endothelial dependent vascular function in atherosclerotic mice en_US
dc.type Thesis en_US
thesis.degree.discipline Physiology (Medicine) en_US
thesis.degree.grantor University of Missouri--Columbia en_US
thesis.degree.name M.S. en_US
thesis.degree.level Masters en_US
dc.relation.ispartofcommunity University of Missouri-Columbia. Graduate School. Theses and Dissertations. Theses. 2012 Theses


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