Low-density lipoprotein and scavenger receptor activities are modulated by secretory products derived from cells of the arterial wall.

The atherosclerotic lesion consists of cholesterol-loaded macrophages, smooth muscle cells, and other cells of the arterial wall. Conditioned medium from human monocyte-derived macrophages (HMDM) stimulated both acetylated and native low-density lipoprotein (Ac-LDL and LDL, respectively) degradation in autologous cells by 25% and 90%, respectively, and this was due to an increase in the number of both LDL and Ac-LDL receptors. Macrophage conditioned medium also resulted in an approximate doubling of LDL degradation by human arterial smooth muscle cells (HASMC), endothelial cells (HEC), and skin fibroblasts (HSF). Macrophage degradation of both Ac-LDL and LDL was enhanced 15% to 45% by conditioned medium derived from HASMC and HSF, respectively, but not by HEC-conditioned medium. Conditioned medium from HASMC, like that from macrophages, could also enhance LDL degradation by smooth muscle cells, fibroblasts, endothelial cells, and macrophages. Thus, the current study demonstrated that arterial wall cells secretory products can affect cellular lipoprotein receptor activities. This phenomenon could lead to increased cellular cholesterol accumulation and foam cell formation.