Advertisement

Research Article Free access | 10.1172/JCI118255

Decreased early atherosclerotic lesions in hypertriglyceridemic mice expressing cholesteryl ester transfer protein transgene.

T Hayek, L Masucci-Magoulas, X Jiang, A Walsh, E Rubin, J L Breslow, and A R Tall

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Hayek, T. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Masucci-Magoulas, L. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Jiang, X. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Walsh, A. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Rubin, E. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Breslow, J. in: JCI | PubMed | Google Scholar

Laboratory of Biochemical Genetics and Metabolism, Rockefeller University, New York 10021-6399, USA.

Find articles by Tall, A. in: JCI | PubMed | Google Scholar

Published October 1, 1995 - More info

Published in Volume 96, Issue 4 on October 1, 1995
J Clin Invest. 1995;96(4):2071–2074. https://doi.org/10.1172/JCI118255.
© 1995 The American Society for Clinical Investigation
Published October 1, 1995 - Version history
View PDF
Abstract

The human cholesteryl ester transfer protein (CETP) facilitates the transfer of cholesteryl ester from HDL to triglyceride-rich lipoproteins. The activity of CETP results in a reduction in HDL cholesterol levels, but CETP may also promote reverse cholesterol transport. Thus, the net impact of CETP expression on atherogenesis is uncertain. The influence of hypertriglyceridemia and CETP on the development of atherosclerotic lesions in the proximal aorta was assessed by feeding transgenic mice a high cholesterol diet for 16 wk. 13 out of 14 (93%) hypertriglyceridemic human apo CIII (HuCIII) transgenic (Tg) mice developed atherosclerotic lesions, compared to 18 out of 29 (62%) controls. In HuCIII/CETPTg, human apo AI/CIIITg and HuAI/CIII/CETPTg mice, 7 of 13 (54%), 5 of 10 (50%), and 5 of 13 (38%), respectively, developed lesions in the proximal aorta (P < .05 compared to HuCIIITg). The average number of aortic lesions per mouse in HuCIIITg and controls was 3.4 +/- 0.8 and 2.7 +/- 0.6, respectively in HuCIII/CETPTg, HuAI/CIIIg, and HuAI/CIII/CETPTg mice the number of lesions was significantly lower than in HuCIIITg and control mice: 0.9 +/- 0.4, 1.5 +/- 0.5, and 0.9 +/- 0.4, respectively. There were parallel reductions in mean lesion area. In a separate study, we found an increased susceptibility to dietary atherosclerosis in nonhypertriglyceridemic CETP transgenic mice compared to controls. We conclude that CETP expression inhibits the development of early atherosclerotic lesions but only in hypertriglyceridemic mice.

Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (October 1, 1995): No description
Advertisement
Advertisement