Depletion of L-cell sterol depresses endocytosis

Abstract

THE engulfment of droplets of fluid, from the surrounding medium (endocytosis or pinocytosis), represents a phenomenon of the plasma membrane of many mammalian cells^1–3. The physiological significance of the process is not well understood although circumstantial evidence seems to suggest that it is necessary for normal functions of certain cell types. Steinman et al.⁴ have established the qualitative and quantitative aspects of endocytosis and have demonstrated that a variety of cells directly interiorise soluble proteins (for example, horseradish peroxidase) by invagination of the plasma membrane without previous binding of the proteins to cell-surface receptors. Cholesterol is a prominent constituent of the plasma membrane of mammalian cells, and its role in many complex functions of the cell membrane is just beginning to be understood. It buffers the ‘fluidity’ of the plasma membrane, increasing the viscosity at high temperatures and inpeding the transition into the gel state at reduced temperatures^5–7. Through its action on membrane fluidity, or possibly more directly, it affects specific functions of the membrane such as ion transport and enzyme activities⁸. With these manifold effects of cholesterol on membrane structure and function in mind, we investigated the effect of altered sterol concentration on the ability of cultured cells to carry out endocytosis, to clarify further the role of cholesterol in membrane-dependent cytological functions.