Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1896
(Arteriosclerosis, Thrombosis, and Vascular Biology. 2005;25:1896.)
© 2005 American Heart Association, Inc.
|
Atherosclerosis and Lipoproteins |
Overexpression of Human Apolipoprotein A-II in Transgenic Mice Does Not Impair Macrophage-Specific Reverse Cholesterol Transport In Vivo
Noemí Rotllan;
Vicent Ribas;
Laura Calpe-Berdiel;
Jesús M. Martín-Campos;
Francisco Blanco-Vaca;
Joan Carles Escolà-Gil
 |
Abstract
|
|---|
Background Overexpression of human apolipoprotein (apo)
A-II in transgenic mice induces high-density lipoprotein (HDL)
deficiency, and increased atherosclerosis susceptibility only
when fed an atherogenic diet. This may, in part, be caused by
impairment in reverse cholesterol transport (RCT).
Methods and Results [3H]cholesterol-labeled macrophages were injected intraperitoneally into mice maintained on a chow diet or an atherogenic diet. Plasma [3H]cholesterol did not differ from human apoA-II transgenic and control mice at 24 or 48 hours after the label injection. On the chow diet, human apoA-II transgenic mice presented increased [3H]cholesterol in liver (1.3-fold) and feces (6-fold) compared with control mice (P<0.05). The magnitude of macrophage-specific RCT did not differ between transgenic and control mice fed the atherogenic diet.
Conclusions Human apoA-II maintains effective RCT from macrophages to feces in vivo despite an HDL deficiency. These findings suggest that the increased atherosclerotic lesions observed in apoA-II transgenic mice fed an atherogenic diet are not caused by impairment in macrophage-specific RCT.
Key Words: apolipoprotein A-II atherosclerosis high-density lipoprotein macrophages reverse cholesterol transport
 |
Web Site Feature
|
|---|
The full-length article can be found on the World Wide Web at
http://www.atvbaha.org