Cyclic AMP mediated modification of cholesterol traffic in Leydig tumor cells.

Abstract

The level of nonesterified cholesterol within MA-10 Leydig Tumor cells is regulated acutely by trophic hormones (Freeman, D. A., and Ascoli, M. (1982) J. Biol. Chem. 257, 14231-14238). In the present studies, we localize the site of this steroidogenic cholesterol to the plasma membrane and characterize the means by which this membrane becomes cholesterol-depleted. It is possible to detect the translocation of both newly synthesized cholesterol and cholesterol derived from lipoproteins from the cell interior to the plasma membrane. Stimulated MA-10 cells that are actively producing steroid hormones divert cholesterol from the normal intracellular or plasma membrane acceptor sites into the steroid biosynthetic pathway. Another important effect of steroidogenic stimulation is to cause internalization of plasma membrane cholesterol. Changes in cholesterol traffic in stimulated cells can be blocked by preventing the utilization of cholesterol for steroidogenesis. This later finding indicates that the changes in cholesterol transport induced by trophic hormones are consequences rather than primary causes of steroidogenic stimulation.