Hyperglycemia does not affect tissue repair responses in shear stress-induced atherosclerotic plaques in ApoE-/- mice.

ABSTRACT: The mechanisms responsible for macrovascular complications in diabetes remain to be fully understood. Recent studies have identified impaired vascular repair as a possible cause of plaque vulnerability in diabetes. This notion is supported by observations of a reduced content of fibrous proteins and smooth muscle cell mitogens in carotid endarterectomy from diabetic patients along with findings of decreased circulating levels of endothelial progenitor cells. In the present study we used a diabetic mouse model to characterize how hyperglycemia affects arterial repair responses. We induced atherosclerotic plaque formation in ApoE-deficient (ApoE-/-) and heterozygous glucokinase knockout ApoE-deficient mice (ApoE-/- GK+/-) mice with a shear stress-modifying cast. There were no differences in

SUBMITTER: Hsiung S 

PROVIDER: S-EPMC5951920 | biostudies-literature | 2018 May

REPOSITORIES: biostudies-literature