Open AccessIncreased atherosclerosis in P2Y13/apolipoprotein E double-knockout mice: contribution of P2Y13 to reverse cholesterol transport
Author(s) -
Laeticia Lichtenstein,
Nizar Serhan,
Sara Espinosa-Delgado,
Aurélie Fabre,
Wijtske Annema,
Uwe J.F. Tietge,
Bernard Robaye,
JeanMarie Boeynaems,
Muriel Laffargue,
Bertrand Perret,
Laurent O. Martinez
Publication year - 2015
Publication title -
cardiovascular research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.774
H-Index - 219
eISSN - 1755-3245
pISSN - 0008-6363
DOI - 10.1093/cvr/cvv109
Subject(s) - apolipoprotein e , scavenger receptor , reverse cholesterol transport , biology , cholesterol , medicine , endocrinology , knockout mouse , receptor , lipoprotein , disease
High-density lipoproteins (HDLs) protect against atherosclerosis mainly due to their function in hepatobiliary reverse cholesterol transport (RCT). This is a process whereby excess cholesterol from peripheral tissues is transported by HDL particles to the liver for further metabolism and biliary excretion. Hepatic uptake of HDL holoparticles involves the P2Y13 receptor, independently of the selective cholesteryl ester uptake mediated by scavenger receptor class B, type I (SR-BI). Accordingly, P2Y13-deficient mice (P2Y13 (-/-)) have impaired RCT. This study assessed whether P2Y13 deficiency would affect atherosclerotic development.
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