Activation of PPARδ prevents endothelial dysfunction induced by overexpression of amyloid-β precursor protein.

ABSTRACT:

Aims

Existing evidence suggests that amyloid-β precursor protein (APP) causes endothelial dysfunction and contributes to pathogenesis of atherosclerosis. In the present study, experiments were designed to: (1) determine the mechanisms underlying endothelial dysfunction and (2) define the effects of peroxisome proliferator-activated receptor delta (PPARδ) ligand on endothelial function in transgenic Tg2576 mice overexpressing mutated human APP.

Methods and results

Confocal microscopy and western blot analyses of wild-type mice aortas provided evidence that APP protein is mainly present in endothelial cells. Overexpression of APP significantly impaired endothelium-dependent relaxations to acetylcholine and phosphorylation of endothelial nitric oxide synthase at Ser(1177) in ao

SUBMITTER: d'Uscio LV 

PROVIDER: S-EPMC3500044 | biostudies-literature | 2012 Dec

REPOSITORIES: biostudies-literature