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(Received for publication, April 4, 1997, and in revised form, July 12, 1997)
,
From the Plasma high density lipoproteins
(HDLs) from humans, from transgenic mice to human apolipoprotein A-I
(HuAITg mice), from transgenic mice to human apolipoprotein A-II
(HuAIITg mice), from transgenic mice to human apolipoproteins A-I and
A-II (HuAIAIITg mice), and from C57BL/6 control mice were isolated, and
their ability to interact with the human cholesteryl ester transfer protein (CETP) was studied. Whereas cholesteryl ester transfer rates
were gradually enhanced by the addition of moderate amounts of HDL from
the different sources, striking differences appeared when HDL levels
kept increasing beyond a maximal transfer value. Indeed, while a
plateau value corresponding to maximal CETP activity was maintained
when raising the concentration of HuAITg HDL and HuAIAIITg HDL,
inhibitions could be observed with the highest levels of human, control
mouse, and HuAIITg mouse HDL. The concentration-dependent inhibition of
CETP activity could be reproduced by the addition of delipidated HDL
apolipoproteins from control mice, but it was abolished by a 1-h
preheating treatment at 56 °C. In contrast, no significant
inhibition of CETP activity was observed with the delipidated protein
moiety of HuAITg HDL, and cholesteryl ester transfer rates remained
unchanged before and after a 1-h, 56 °C preheating step. Finally,
the CETP-mediated transfer of radiolabeled cholesteryl esters from
human low density lipoprotein to human HDL was significantly higher in
the presence of lipoprotein-deficient plasma from HuAITg mice than in
the presence of lipoprotein-deficient plasma from control mice.
Interestingly, cholesteryl ester transfer rates measured with both
control and HuAITg lipoprotein-deficient plasmas became remarkably
similar following a 1-h, 56 °C preheating treatment.
It is concluded that human, control mouse, and HuAIITg mouse HDL
contain a heat-labile lipid transfer inhibitory activity that is absent
from HDL of HuAITg and HuAIAIITg mice. Alterations in CETP-lipoprotein
binding did not account for differential lipid transfer inhibitory
activities.
Laboratoire de Biochimie des
Lipoprotéines, INSERM CJF 93-10, Faculté de
Médecine, 21033 Dijon Cedex, France and the § Centre
de Recherches de Vitry-Alfortville, Rhône-Poulenc Rorer, Gencell
Division, Atherosclerosis Department,
94403 Vitry-sur-Seine Cedex, France
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