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Correspondence to:
Francisco Blanco-Vaca.
We report on the effect of human apolipoprotein (apo) A-II transgene expression on atherosclerosis susceptibility in two transgenic lines (25.3 and 11.1) whose plasma human apoA-II concentrations (~23 and 96 mg/dl, respectively) span the normal range in humans. After 9 months of an atherogenic diet, 25.3 and 11.1 transgenic mice developed aortic atherosclerotic lesions that were ~1.7- and 7-fold, respectively, more extensive than those of nontransgenic control mice. However, there was no difference in the area of atherosclerosis of transgenic and control mice when fed a regular chow diet. This contrasts with the findings in murine apoA-II transgenic mice and provides evidence of a species-specific characteristic that could be of relevance with respect to the high fat intake diets common in most industrialized countries. A possible mechanism of the pro-atherogenic action of human apoA-II could be the inhibition of reverse cholesterol transport and, in support of this, we observed an impairment of apoA-I-HDL particle interconversion in the plasma of 11.1 transgenic mice caused, at least in part, by a marked decrease in the endogenous lecithin:cholesterol acyltransferase activity.—Escolà-Gil, J. C., À. Marzal-Casacuberta, J. Julve-Gil, B. Y. Ishida, J. Ordóñez-Llanos, L. Chan, F. González-Sastre, and F. Blanco-Vaca. Human apolipoprotein A-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: evidence of a potentially relevant species-specific interaction with diet. J. Lipid Res. 1998. 39: 457–462.
Supplementary key words:
high density lipoproteins, atherosclerosis, apolipoprotein A-I, lecithin:cholesterol acyltransferase
Copyright © 1998 by Lipid Research, Inc.
Rapid Communication
Human apolipoprotein A-II is a pro-atherogenic molecule when it is expressed in transgenic mice at a level similar to that in humans: evidence of a potentially relevant species-specific interaction with diet
Joan Carles Escolà-Gila,b,
Àfrica Marzal-Casacubertaa,b,c,
Josep Julve-Gila,b,
Brian Y. Ishidad,
Jordi Ordóñez-Llanosa,c,
Lawrence Chane,
Francesc González-Sastrea,c, and
Francisco Blanco-Vacaa,b
a Servei de Bioquímica, Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
b Institut de Recerca de l'Hospital de la Santa Creu i Sant Pau, Barcelona, Spain
c Departament de Bioquímica i Biologia Molecular, Universitat Autònoma de Barcelona, Barcelona, Spain
d Department of Medicine, University of California-San Francisco, San Francisco, CA
e Departments of Cell Biology and Medicine, Baylor College of Medicine, Houston, TX
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