Faculty mentor: J. David Symons
We tested the hypothesis that deleting ceramide biosynthesis specifically in endothelial cells (ECs) attenuates obesity-induced arterial dysfunction. Metabolic and vascular phenotyping was completed using wild type mice and mice with EC-specific deletion of Sptlc2 that consumed standard or high fat chow for 14-weeks. Preliminary results indicate obesity-induced metabolic and vascular disruptions are not attenuated by EC-specific Sptlc2 deletion.
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