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Research Article Free access | 10.1172/JCI117614

Human ApoA-II inhibits the hydrolysis of HDL triglyceride and the decrease of HDL size induced by hypertriglyceridemia and cholesteryl ester transfer protein in transgenic mice.

S Zhong, I J Goldberg, C Bruce, E Rubin, J L Breslow, and A Tall

Department of Medicine, Columbia University, New York 10032.

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Department of Medicine, Columbia University, New York 10032.

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Department of Medicine, Columbia University, New York 10032.

Find articles by Bruce, C. in: JCI | PubMed | Google Scholar

Department of Medicine, Columbia University, New York 10032.

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

Department of Medicine, Columbia University, New York 10032.

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Department of Medicine, Columbia University, New York 10032.

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Published December 1, 1994 - More info

Published in Volume 94, Issue 6 on December 1, 1994
J Clin Invest. 1994;94(6):2457–2467. https://doi.org/10.1172/JCI117614.
© 1994 The American Society for Clinical Investigation
Published December 1, 1994 - Version history
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Abstract

The plasma cholesteryl ester transfer protein (CETP) mediates the exchange of HDL cholesteryl esters with triglycerides of other lipoproteins. Subsequent lipolysis of the triglyceride-enriched HDL by hepatic lipase leads to reductions of HDL size and apoA-I content. To investigate a possible modulation of the effects of CETP by apoA-II, human CETP transgenic mice were cross-bred with transgenic mice expressing human apoA-II and, in some cases, human apoA-I and apoC-III (with human-like HDL and hypertriglyceridemia). CETP expression resulted in reductions of HDL and increases in VLDL cholesteryl ester in mice expressing human apoA-II, alone or in combination with apoA-I and apoC-III, indicating that apoA-II does not inhibit the cholesteryl ester transfer activity of CETP. However, CETP expression resulted in more prominent increases in HDL triglyceride in mice expressing both apoA-II and CETP, especially in CETP/apoA-II/apoAI-CIII transgenic mice. CETP expression caused dramatic reductions in HDL size and apoA-I content in apoAI-CIII transgenic mice, but not in apoA-II/AI-CIII transgenic mice. HDL prepared from mice of various genotypes showed inhibition of emulsion-based hepatic lipase activity in proportion to the apoA-II/apoA-I ratio of HDL. The presence of human apoA-II also inhibited mouse plasma hepatic lipase activity on HDL triglyceride. Thus, apoA-II does not inhibit the lipid transfer activity of CETP in vivo. However, coexpression of apoA-II with CETP results in HDL particles that are more triglyceride enriched and resistant to reductions in size and apoA-I content, reflecting inhibition of hepatic lipase by apoA-II. The inhibition of HDL remodeling by apoA-II could explain the relatively constant levels of HDL containing both apoA-I and apoA-II in human populations.

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Referenced in 2 patents
11 readers on Mendeley
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