Very low and intermediate density lipoprotein fractions from apolipoprotein E gene-knockout mice induce cholesteryl ester accumulation in J774 macrophages.

OBJECTIVE

To investigate the atherogenic role of very low density lipoprotein (VLDL) and intermediate density lipoprotein (IDL) fraction isolated from plasma of apolipoprotein E (apoE)-knockout mice.

METHODS

Containing both VLDL and IDL (apoEko-VLDL/IDL), lipoprotein fraction was isolated from plasma of apoE-knockout mice by ultracentrifugation, and its interaction with J774 macrophages was examined together with its physicochemical properties including lipid content, electrophoresis mobility and apolipoprotein components.

RESULTS

ApoEko-VLDL/IDL could be actively taken up by J774 macrophages, resulting in marked cholesterol ester accumulation in the cells (55 +/- 9 nmol/mg cell protein), which was a 7-fold increase over the corresponding lever induced by low density lipoprotein and significantly higher than non-loaded group (P < 0.01).

CONCLUSION

ApoEko-VLDL/IDL induced significant cholesterol ester accumulation through an apoE independent pathway. This pathway may explain, partly the mechanism of cholesterol deposition in arterial wall in apoE-knockout mice.