Cholesterol levels inversely reflect the thermal sensitivity of mammalian cells in culture

Abstract

Cholesterol is a primary component of the mammalian cell plasma membrane. Although its function is unknown, it may be of major importance in maintaining membrane fluidity and rigidity¹. In artificial membrane systems, the addition of cholesterol results in a condensing effect—thickening the bilayer and inducing higher order in the acyl chains of the phospholipids². Permeability profiles indicate that the addition of cholesterol into egg–lecithin bilayers increases the half-time of solute transport³. In addition, decreased amounts of sterol in the membrane increase glucose permeability, and, in L cells, increase the transport of rubidium^4,5. These studies suggest a role for cholesterol in changing the physical characteristics of the membrane resulting in the alteration of membrane permeability. We now provide evidence that cholesterol may act, presumably via changes in physical membrane properties, with yet another biological consequence; regulating the survival sensitivity of mammalian cells to hyperthermic temperatures.