Endothelial Cell-Specific Deletion of P2Y2 Receptor Promotes Plaque Stability in Atherosclerosis-Susceptible ApoE-Null Mice.

ABSTRACT:

Objective

Nucleotide P2Y₂ receptor (P2Y₂R) contributes to vascular inflammation by increasing vascular cell adhesion molecule-1 expression in endothelial cells (EC), and global P2Y₂R deficiency prevents fatty streak formation in apolipoprotein E null (ApoE^-/-) mice. Because P2Y₂R is ubiquitously expressed in vascular cells, we investigated the contribution of endothelial P2Y₂R in the pathogenesis of atherosclerosis.

Approach and results

EC-specific P2Y₂R-deficient mice were generated by breeding VEcadherin5-Cre mice with the P2Y₂R floxed mice. Endothelial P2Y₂R deficiency reduced endothelial nitric oxide synthase activity and significantly altered ATP- and UTP (uridine 5'-triph

SUBMITTER: Chen X 

PROVIDER: S-EPMC5268079 | biostudies-literature | 2017 Jan

REPOSITORIES: biostudies-literature