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J. Biol. Chem., Vol. 277, Issue 35, 31354-31363, August 30, 2002
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From the Transgenic mice expressing human
cholesteryl ester transfer protein (HuCETPTg mice) were crossed with
apolipoprotein CI-knocked out (apoCI-KO) mice. Although total
cholesterol levels tended to be reduced as the result of CETP
expression in HuCETPTg heterozygotes compared with C57BL6 control mice
(
Apolipoprotein CI Deficiency Markedly Augments Plasma Lipoprotein
Changes Mediated by Human Cholesteryl Ester Transfer Protein (CETP) in
CETP Transgenic/ApoCI-knocked Out Mice*
,,,,,,,,,
,
Laboratoire de Biochimie des
Lipoprotéines, INSERM U498, Faculté de Médecine,
BP87900, 21079 Dijon Cedex, France, § Netherlands
Organization for Applied Scientific Research (TNO), Prevention and
Health, Gaubius Laboratory, 2301 CE Leiden, The Netherlands,
** Departments of Cardiology and General Internal
Medicine, Leiden University Medical Center, Leiden, The
Netherlands, ¶ State University of New York, Downstate Medical
Center, Brooklyn, New York 11203, and Division of Molecular
Medicine, Department of Medicine, Columbia University,
New York, New York 10032
13%, not significant), a more pronounced decrease (28%,
p < 0.05) was observed when human CETP was expressed
in an apoCI-deficient background (HuCETPTg/apoCI-KO mice). Gel
permeation chromatography analysis revealed a significant, 6.1-fold
rise (p < 0.05) in the cholesteryl ester content of
very low density lipoproteins in HuCETPTg/apoCI-KO mice compared with control mice, whereas the 2.7-fold increase in HuCETPTg
mice did not reach the significance level in these experiments.
Approximately 50% decreases in the cholesteryl ester content and
cholesteryl ester to triglyceride ratio of high density lipoproteins
(HDL) were observed in HuCETPTg/apoCI-KO mice compared with controls (p < 0.05 in both cases), with intermediate 20%
changes in HuCETPTg mice. The cholesteryl ester depletion of HDL was
accompanied with a significant reduction in their mean apparent
diameter (8.68 ± 0.04 nm in HuCETPTg/apoCI-KO mice
versus 8.83 ± 0.02 nm in control mice;
p < 0.05), again with intermediate values in HuCETPTg
mice (8.77 ± 0.04 nm). In vitro purified apoCI was
able to inhibit cholesteryl ester exchange when added to either total
plasma or reconstituted HDL-free mixtures, and coincidently, the
specific activity of CETP was significantly increased in the
apoCI-deficient state (173 ± 75 pmol/µg/h in HuCETPTg/apoCI-KO
mice versus 72 ± 19 pmol/µg/h in HuCETPTg,
p < 0.05). Finally, HDL from apoCI-KO mice were shown
to interact more readily with purified CETP than control HDL that
differ only by their apoCI content. Overall, the present observations
provide direct support for a potent specific inhibition of CETP by
plasma apoCI in vivo.
*
This work was supported by the Université de
Bourgogne, the Conseil Régional de Bourgogne, the INSERM, and the
Fondation de France.The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
To whom correspondence should be addressed. Tel.:
33-3-80-39-32-63; Fax: 33-3-80-39-34-47; E-mail:
laurent.lagrost@u-bourgogne.fr.
Copyright © 2002 by The American Society for Biochemistry and Molecular Biology, Inc.
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