Cholesterol efflux from and high-density-lipoproteins binding to cultured bovine vascular endothelial cells are higher than with vascular smooth muscle cells.

Cholesterol metabolism was studied and compared in confluent cultures of adult bovine aortic endothelial and bovine aortic smooth muscle cells which were grown under similar conditions. The total cholesterol content/mg protein was only slightly higher in smooth muscle cells than in endothelial cells and upon exposure to [3H]cholesterol the maximal specific activity/mg protein obtained was similar in both cell types. Most (98%) of the incorporated [3H]cholesterol remained in the form of free cholesterol in both cell types, and provided a system for the study of cholesterol efflux. The role of high-density lipoproteins (HDL) and human serum in cholesterol influx and efflux, in both endothelial and smooth muscle cells, was studied. Net cholesterol transport in the cultures was calculated and net efflux was observed in both cell types. This was higher in endothelial than in smooth muscle cells and HDL was more efficient than human serum in promoting net cholesterol efflux. During the influx experiments, no conversion of [3H]cholesterol to [3H]cholesteryl ester was observed either in the cell layer or in the incubation medium. On the other hand, during efflux experiments when HDL but not human serum was the acceptor, some (about 6%) conversion of [3H]cholesterol to [3H]cholesteryl ester occurred in the incubation medium. 125I-HDL3 binding to endothelial and smooth muscle cells was studied and demonstrated saturation at a concentration of about 100 micrograms protein/ml for both cell types. However, endothelial cells bound about six times more 125I-HDL3 than smooth muscle cells. These studies indicate that vascular endothelial cells are more protected against cholesterol accumulation than vascular smooth muscle cells. The greater ability of endothelial cells to bind HDL complexes when compared with smooth muscle cells, and thereby to be more susceptible to HDL induced cholesterol efflux, may add a new mechanism through which endothelial cells protect the blood vessel from cholesterol accumulation.