Interaction of lipoproteins with macrophages.

Abstract

The suggestion that the cholesterol accumulation in cardiovascular lesions is caused by an interaction of serum lipoproteins with arterial cells has been supported by numerous investigations. The lipid-loaden foam cells which accumulate cholesterol in atheroma are thought to arise from either smooth muscle cells [1–4] or monocytes-macrophages [1,2,5,6]. At the present time, however, it has not been possible to demonstrate that smooth muscle cells can be overloaded with cholesterol by any of the naturally occurring or cholesterol-induced lipoproteins. These cells, like fibroblasts, lymphocytes and endothelial cells, can prevent excessive uptake and accumulation of lipoprotein-cholesterol due to the presence of specific cell surface receptors for plasma lipoproteins [7]. The binding of the lipoproteins to these receptors initiates a number of intracellular events, including internalization and degradation of the lipoproteins and the subsequent regulation of cellular cholesterol metabolism. The receptors interact with both low density lipoproteins (LDL), which contain the B-apoprotein, and certain high density lipoproteins (HDL), which contain the E-apoprotein, and are, therefore, designated as apo B, E receptors [8, 9].