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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

Atheroprotective potential of macrophage-derived phospholipid transfer protein in low-density lipoprotein receptor-deficient mice is overcome by apolipoprotein AI overexpression.

OBJECTIVE: Using bone marrow transplantation, we assessed the impact of macrophage-derived phospholipid transfer protein ( PLTP) on lesion development in hypercholesterolemic mice that expressed either normal levels of mouse apolipoprotein AI (apoAI) or elevated levels of only human apoAI. METHODS AND RESULTS: Bone marrow transplantations were performed in low-density lipoprotein receptor-deficient mice (LDLr-/-) that expressed either normal levels of mouse apoAI (msapoAI) or high levels of only human apoAI (msapoAI-/-, LDLr-/-, huapoAITg). Mice were lethally irradiated, reconstituted with either PLTP-expressing or PLTP-deficient bone marrow cells, and fed a high-fat diet over 16 weeks. Macrophage PLTP deficiency increased atherosclerosis in LDLr-/- mice with minimal changes in total plasma cholesterol levels. In contrast, the extent of atherosclerosis in msapoAI-/-, LDLr-/-, huapoAITg mice was not significantly different between groups that had received PLTP-/- or PLTP+/+ bone marrow. In vitro studies indicated that PLTP deficiency led to a significant decrease in alpha-tocopherol content and increased oxidative stress in bone marrow cells. CONCLUSIONS: Our observations suggest an atheroprotective role of macrophage-derived PLTP in mice with normal apoAI plasma levels. The atheroprotective properties of macrophage-derived PLTP were not observable in the presence of elevated plasma concentrations of apoAI.[1]

References

  1. Atheroprotective potential of macrophage-derived phospholipid transfer protein in low-density lipoprotein receptor-deficient mice is overcome by apolipoprotein AI overexpression. Valenta, D.T., Ogier, N., Bradshaw, G., Black, A.S., Bonnet, D.J., Lagrost, L., Curtiss, L.K., Desrumaux, C.M. Arterioscler. Thromb. Vasc. Biol. (2006) [Pubmed]
 
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