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Papers In Press, published online ahead of print July 16, 2004
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Anatomy and Cell Biology, SUNY, Brooklyn, NY 11203
Corresponding Author: xjiang{at}downstate.edu
We previously reported that phospholipid transfer protein deficiency (PLTP0) decreased atherosclerosis in mouse models. Since the decreased atherosclerosis was accompanied by a significant decrease in plasma HDL levels, we examined the properties of PLTP0 HDL and tested its ability to prevent LDL-induced monocyte chemotactic activity in human artery wall cell cocultures. We isolated HDL and LDL from LDL receptor and PLTP double knock out (LDLr0/PLTP0) mice and from apoB transgenic (apoBTg)/PLTP0 mice as well as from their controls, i.e. LDLr0 and apoBTg mice, respectively. We found that PLTP0 HDL was relatively rich in protein and depleted in phosphatidylcholine. Turnover studies using autologous HDL revealed a 3.5 to 4.0-fold increase in the turnover of protein and cholesteryl ester in HDL from PLTP0 mice compared to control. The ability of HDL from LDLr0/PLTP0 and apoBTg/PLTP0 mice to prevent the induction of monocyte chemotactic activity in human artery wall cell cocultures exposed to human LDL was dramatically better than controls. Moreover, LDL from PLTP0 mice was markedly resistant to oxidation and induced significantly less monocyte chemotactic activity when presented to human artery wall cells compared to controls. In vitro, PLPT0 HDL removed significantly more oxidized phospholipids from LDL than control HDL. We conclude that PLTP deficiency improves the anti-inflammatory properties of HDL in mice and reduces the ability of LDL to induce monocyte chemotactic activity.
Revised on June 24, 2004
Accepted on July 7, 2004
Phospholipid transfer protein deficiency improves the anti-inflammatory properties of high density lipoprotein and reduces the ability of low density lipoprotein to induce monocyte chemotactic activity
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