The receptor—mediated accumulation of triglyceride in macrophage exposed to very low density lipoproteins

Abstract

VLDLs isolated from the normolipidemic rat or monkey and the hyperlipidemic rat stimulated the incorporation of₁₄C-oleic acid into triglyceride of the mouse peritoneal macrophages. The magnitude of this stimulating effect depended upon the concentration of lipoproteins in the medium. Experiments using₁₂₅I labeled VLDLs revealed that the binding of normolipidemic VLDL with the macrophage was saturable, and unlabeled VLDL competed effectively with the labeled VLDL. These results suggested that on the surface of the macrophages there are special binding sites for the VLDL. It is possible that separate receptors are responsible for either the normolipidemic or the hyperlipidemic VLDL.

The hyperlipidemic VLDL from rat or monkey enhanced the synthesis of₁₄C-cholesterol ester. After binding with the macrophage, the different VLDLs caused accumulation of either triglyceride or cholesterol ester or both. The possible interpretation is that it depends upon the lipid composition of that VLDL, especially the ratio of triglyceride versus cholesterol ester.

The present study supports the concept that at least a part of the foam cells derive from the macrophage, i.e., the macrophage plays an important role in the formation of the atherosclerotic lesion. In addition, the binding and degradation of the normolipidemic VLDL by the macrophage may be of physiological importance in the metabolism of VLDL.

Keywords

macrophage / very low density lipoprotein / triglyceride

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