ABSTRACT
The red blood cell, as it continuously circulates, must be able to undergo extensive deformation and to resist fragmentation. These two essential qualities require a highly deformable yet remarkably stable membrane. Membrane deformability and mechanical stability appear to be regulated by an extensive network of structural proteins that underlies the lipid bilayer and is associated with it by protein-protein and protein-lipid interactions [1–3]. When the integrity of the membrane skeleton is disrupted by structural abnormalities or deficiencies of its protein components, the membrane becomes susceptible to fragmentation and the red blood cells in turn lose their characteristic discoid shape. Evidence to support this contention has been derived from membrane stability studies of red blood cells from patients with defined quantitative or qualitative skeletal protein abnormalities [2,4–12].
