A mechanism by which high-density lipoproteins may slow the atherogenic process.

There is a well-documented negative correlation between plasma concentrations of high-density lipoproteins (H.D.L.) and risk of clinically evident atherosclerosis. This may relate to the postulated role of H.D.L. in the transport of cholesterol out of cells. Studies of the metabolism of lipoproteins by arterial smooth-muscle cells suggest that a second mechanism also operates, H.D.L. binds to the surface of porcine arterial smooth-muscle cells as effectively as low-density lipoprotein (L.D.L.) but is internalised and degraded much more slowly. When incubated with L.D.L. these cells show a net increment in cholesterol content. However, cells incubated with equal or higher concentration of H.D.L. under comparable conditions show no cholesterol accumulation. The presence of H.D.L. in the medium partially inhibits uptake and degradation of L.D.L. and, most important, also partially suppresses the net increment in cell sterol content induced by L.D.L. The demonstrated interaction of H.D.L. and L.D.L. could be a second mechanism contributing to the apparent protective effect of high plasma-H.D.L. concentrations in relation to atherogenesis.