High-Density Lipoprotein and the Dynamics of

Plump et al1 reported in 1994 that the expression of ahuman transgene for apoA-I, the major apolipoproteinof HDL, in apoE knockout mice dramatically reduced lesion formation. In the present issue of Circulation, Rong et al2 demonstrate that the composition and structure of ad-vanced atherosclerotic plaques can be significantly altered by the expression of this same transgene. Rong and colleagues2 used a novel transplant model. They fed apoE knockout mice a Western diet for 6 months to generate advanced lesions. Subsequently, they surgically removed portions of the aorta from these mice and transplanted them into the aortas of syngeneic mice on a chow diet, some of which also expressed the transgene for human apoA-I. The recipient mice express-ing the human transgene had 2.5-fold higher HDL choles-terol levels and expressed 13015 mg/dL of human apoA-I. The non-HDL cholesterol levels were approximately half of those that had been present in the donor mice and wer