Correction for Arterioscler Thromb Vasc Biol 22 (5) 878.

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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:1243.)
© 2002 American Heart Association, Inc.

In the PDF of the abstracts presented at the 3rd Annual Conference on Arteriosclerosis, Thrombosis, and Vascular Biology (Arteriosclerosis, Thrombosis, and Vascular Biology. 2002;22:878 -a), abstract P138, "Deficiency of Adipocyte Fatty Acid-Binding Protein aP2 Is Protective in the ApoE-Deficient Mice on Western Diet With Advanced Atherosclerosis," was incorrectly listed as withdrawn.

The abstract is listed below.

P138

Deficiency of the Adipocyte Fatty Acid-Binding Protein aP2 Is Protective in ApoE-Deficient Mice on Western Diet with Advanced Atherosclerosis

Jeffrey B Boord, Kazuhisa Maeda, Vladimir R Babaev, Liza Makowski, Tianli Zhu, Z C Gorgun, Sergio Fazio, Macrae F Linton, Gokhan S Hotamisligil. Vanderbilt University Medical Center, Nashville, TN; Harvard School of Public Health, Boston, MA

The adipocyte fatty acid-binding protein aP2 is expressed in both adipocytes and macrophages. Deficiency of aP2 increases insulin sensitivity in obese but not lean mice. We have previously shown that expression of aP2 in macrophages enhances early foam cell formation and atherosclerosis in apoE-deficient mice on chow diet. The determine if aP2 deficiency has a similar effect in the setting of severe hypercholesterolemia and extensive aortic atherosclerosis, four-week-old male and female aP2^-/-apoE^-/- (n=8 male/19 female) mice and age-matched apoE^-/- (n=13 male/14 female) controls were placed on a Western diet (21% fat, 0.15% cholesterol, no cholate) for 14 weeks. After 14 weeks on Western diet, there were no significant differences between male aP2^-/-apoE^-/- and apoE^-/- mice in fasting serum cholesterol (857±103 vs 865±175; mg/dl±SD; p=0.91), triglycerides (183±58 vs 218±99; mg/dl±SD; p=0.38), or glucose (118±90 vs 132±48; mg/dl±SD; p=0.66). There were no significant differences between the female aP2^-/-apoE^-/- and apoE^-/- mice in serum cholesterol (632±54 vs 636±93; mg/dl±SD; p=0.85), triglycerides (140±57 vs 177±76; mg/dl±SD; p=0.12), or glucose (173±63 vs 170±37; mg/dl±SD; p=0.72). Insulin sensitivity by insulin tolerance testing was also similar between groups for each sex. In males, there was a 29% reduction in atherosclerotic lesion area in the proximal aorta (248425±19269 vs 350258–19375; µm²/section±SEM; p=0.002), and a 48% reduction in the en face aorta (0.88±0.29 vs 1.69±0.23; % lesion area±SEM; p=0.04) in aP2^-/-apoE^-/- mice compared to controls. In females there was a 17% reduction in atherosclerotic lesion area in the proximal aorta (370136±13666 vs 447566±24411; µm²/section±SEM; p=0.006), and a 39% reduction in the en face aorta (1.19±0.13 vs 1.97±0.37; % lesion area±SEM; p=0.03) in aP2^-/-apoE^-/- mice compared to controls. We conclude that aP2 deficiency in the setting of severe hypercholesterolemia reduces atherosclerotic lesion formation in apoE^-/- mice, without significant effects on serum lipids or insulin sensitivity.

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