Reduced ABCA1-mediated cholesterol efflux and accelerated atherosclerosis in apolipoprotein E-deficient mice lacking macrophage-derived ACAT1.
AUTHORS
Su
YRYan Ru ,
Dove
DE Dwayne E ,
Major
AS Amy S ,
Hasty
AH Alyssa H ,
Boone
B Branden ,
Linton
MF MacRae F ,
Fazio
S Sergio .
Circulation. 2005 5 10; 111(18).
2373-81
- PMID: 15851589[PubMed].
ABSTRACT
Macrophage acyl-coenzyme A:cholesterol acyltransferase 1 (ACAT1) and apolipoprotein E (apoE) have been implicated in regulating cellular cholesterol homeostasis and therefore play critical roles in foam cell formation. Deletion of either ACAT1 or apoE results in increased atherosclerosis in hyperlipidemic mice, possibly as a consequence of altered cholesterol processing. We have studied the effect of macrophage ACAT1 deletion on atherogenesis in apoE-deficient (apoE-/-) mice with or without the restoration of macrophage apoE.