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Original Article |
Correspondence to: Christian Ehnholm.
To study the function of plasma phospholipid transfer protein (PLTP) in vivo, a liver directed adenoviral gene transfer system was used to overexpress human PLTP in mice. For the experiments, two strains of mice, wild type (C57/Bl) and mice transgenic for the human apoA-I gene (HuApoA-ITg), were utilized. Five days after injection of the recombinant PLTP adenovirus, wild type mice showed a 4 -fold increase in serum PLTP activity in (12.2 ± 1.3 µmol/ml/per h to 48.1 ± 8.6 µmol/ml per h (+394%), P < 0.001). The PLTP overexpression induced significant reduction of serum cholesterol (2.46 ± 0.08 to 0.69 ± 0.42 mmol/l (-72%), P < 0.001), phospholipids (3.10 ± 0.06 to 0.90 ± 0.24 mmol/l (-71%), P < 0.01), and triglycerides (0.2 ± 0.07 to 0.08 ± 0.03 mmol/l (-69%), (P < 0.001). ApoA-I was hardly detectable in the serum. These lipid changes were due to a dramatic reduction of high density lipoprotein (HDL). The HuApoA-ITg mice displayed higher basal HDL level and PLTP activity. Adenovirus mediated PLTP overexpression in these mice resulted in a similar decrease of the lipid levels as that seen in the C57/Bl mice. However, the lipoprotein profile revealed a redistribution of HDL, with the appearance of larger buoyant HDL species.
The results demonstrate that plasma phospholipid transfer protein in vivo causes high density lipoprotein (HDL) conversion and thereby plays a central role in HDL metabolism.—Ehnholm, S., K. Willems van Dijk, B. van 't Hof, A. van der Zee, V. M. Olkkonen, M. Jauhiainen, M. Hofker, L. Havekes, and C. Ehnholm. Adenovirus-mediated overexpression of human phospholipid transfer protein alters plasma HDL levels in mice. J. Lipid Res. 1998. 39: 1248–1253.
Supplementary key words: recombinant adenovirus, phospholipid transfer protein, HDL metabolism, HDL conversion, apolipoprotein A-I, lipid metabolism
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