Open AccessEndothelial Cell–Specific Deletion of P2Y 2 Receptor Promotes Plaque Stability in Atherosclerosis-Susceptible ApoE-Null Mice
Author(s) -
Xingjuan Chen,
Shaomin Qian,
April M. Hoggatt,
Hongying Tang,
Timothy A. Hacker,
Alexander G. Obukhov,
Paul Herring,
Cheikh I. Seye
Publication year - 2016
Publication title -
arteriosclerosis thrombosis and vascular biology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.007
H-Index - 270
eISSN - 1524-4636
pISSN - 1079-5642
DOI - 10.1161/atvbaha.116.308561
Subject(s) - apolipoprotein e , knockout mouse , p2y receptor , endocrinology , fatty streak , inflammation , medicine , uridine triphosphate , endothelial stem cell , endothelial dysfunction , biology , nitric oxide , receptor , chemistry , biochemistry , purinergic receptor , cholesterol , nucleotide , gene , disease , in vitro
Nucleotide P2Y 2 receptor (P2Y 2 R) contributes to vascular inflammation by increasing vascular cell adhesion molecule-1 expression in endothelial cells (EC), and global P2Y 2 R deficiency prevents fatty streak formation in apolipoprotein E null (ApoE -/- ) mice. Because P2Y 2 R is ubiquitously expressed in vascular cells, we investigated the contribution of endothelial P2Y 2 R in the pathogenesis of atherosclerosis.
Accelerating Research
Robert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom
Address
John Eccles HouseRobert Robinson Avenue,
Oxford Science Park, Oxford
OX4 4GP, United Kingdom