Abstract
Highly lipid laden cells, foam cells have long been a characteristic feature of the athersclerotic lesion in man (1). A number of studies in animal models have established that at least a portion of the foam cells are derived from monocyte/macrophages which leave the circulation and enter the arterial wall (2–5). A mechanism whereby macrophages could be converted to foam cells in vitro was elucidated by Goldstein and coworkers. Acetylated low density lipoproteins were able to induce massive cholesteryl ester loading in macrophages as compared to unmodified low density lipoproteins, giving them the appearance of foam cells (6,7). Additional reactions which result in charge modification of lipoproteins have been identified and include malondialdehyde modification (8,9) and oxidation of lipoproteins (10,11). In addition, maeylation of albumin also produces a protein which interacts with the macrophage and competes with the charge modified lipoproteins (12,13). The protein to which these proteins bind has been termed the macrophage scavenger receptor (12). The receptor is demonstrable in foam cells isolated from arterial lesion of cholesterol fed rabbits (14). In vivo, the receptor rapidly clears injected charge modified lipoproteins, with the liver endothelial cells being the primary target cells for uptake (15,16).
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