ABSTRACT
The membrane of the human erythrocyte is reinforced along its entire cytoplasmic surface by a two-dimensional network of peripheral proteins that closely adhere to the membrane proper through specific protein-protein interactions [1–9]. This durable, flexible, and elastic network functions to stabilize the membrane bilayer without compromising its deformability [10–14], thus enabling the red blood cell to withstand the shear stress during its turbulent passage through the vasculature. The erythrocytes respond to the mechanical pressure by transient deformation while traversing through microcapillaries and subsequently return to the biconcave disk shape. This rapid, reversible deformation of the erythrocytes allows for maximum contact between the erythrocyte membrane and the wall of the microcapillaries, thus facilitating the exchange of oxygen and electrolytes while maintaining minimum viscosity in the circulatory system. Perturbations of the skeleton have been shown to cause irreversible alterations in the permeability, integrity, deformation, and shape of cells, leading to red blood cell pathophysiology [15–18].
