Cholesterol levels inversely reflect the thermal sensitivity of mammalian cells in culture.
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 rigidity. 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 phospholipids. Permeability profiles indicate that the addition of cholesterol into egg-lecithin bilayers increases the half-time of solute transport. In addition, decreased amounts of sterol in the membrane increase glucose permeability, and, in L cells, increase the transport of rubidium. 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.
D000818:Animals; D002470:Cell Survival; D002478:Cells, Cultured; D002784:Cholesterol / Q000502:physiology*; D005227:Fatty Acids / Q000502:physiology; D005231:Fatty Acids, Unsaturated / Q000502:physiology; D006358:Hot Temperature; D006801:Humans; D008560:Membrane Fluidity; D008563:Membrane Lipids / Q000502:physiology*; D008565:Membrane Proteins / Q000502:physiology; D010743:Phospholipids / Q000502:physiology
D005227:Fatty Acids; D005231:Fatty Acids, Unsaturated; D008563:Membrane Lipids; D008565:Membrane Proteins; D010743:Phospholipids; D002784:Cholesterol