Remodeling the shape of the skeleton in the intact red cell

Abstract

The role of the membrane skeleton in determining the shape of the human red cell was probed by weakening it in situ with urea, a membrane-permeable perturbant of spectrin. Urea by itself did not alter the biconcave disk shape of the red cell; however, above threshold conditions (1.5 M, 37 degrees C, 10 min), it caused an 18% reduction in the membrane elastic shear modulus. It also potentiated the spiculation of cells by lysophosphatidylcholine. These findings suggest that the contour of the resting cell is not normally dependent on the elasticity of or tension in the membrane skeleton. Rather, the elasticity of the skeleton stabilizes membranes against deformation. Urea treatment also caused the projections induced both by micropipette aspiration and by lysophosphatidylcholine to become irreversible. Furthermore, urea converted the axisymmetric conical spicules induced by lysophosphatidylcholine into irregular, curved and knobby spicules; i.e., echinocytosis became acanthocytosis. Unlike controls, the ghosts and membrane skeletons obtained from urea-generated acanthocytes were imprinted with spicules. These data suggest that perturbing interprotein associations with urea in situ allowed the skeleton to evolve plastically to accommodate the contours imposed upon it by the overlying membrane.

Numerical simulation of the motion of red blood cells and vesicles in microfluidic flows

“…Observing (42) in (47) and (43) in (52), (53) and estimating the remaining terms on the right-hand side in (48) from above as in the proof of Theorem 3.1 allows to conclude. (43) with that for the FE/BE FE-IBM without bending energy (cf., e.g., [12]) shows that (43) imposes a more restrictive bound on the time step size due to the impact of the bending energy.…”

“…(43) with that for the FE/BE FE-IBM without bending energy (cf., e.g., [12]) shows that (43) imposes a more restrictive bound on the time step size due to the impact of the bending energy.…”

“…The blood flow is not only controlled by the viscosity of the plasma [26], but additionally viscoelastic effects due to the deformability of the erythrocytes [15,21], aggregation of the cells [23] and hematocrit have to be taken into account as experimentally observed in the seminal work [37] (cf. also [20,35,39,43,48,49,67,72,[75][76][77]). …”

Quantitative assessment of sensing and sequestration of spherocytic erythrocytes by the human spleen

“…6,7 By initially accumulating exclusively in the external leaflet of the RBC lipid bilayer, LPC induces in a dose-dependent manner echinocytosis (spiculation) and eventually spherocytes through the release of microvesicles. 21,22 The effects of LPC on RBC morphology, surface area loss and S/V ratio, 7,8,21,22 and cellular deformability 6,7,23,24 have been documented extensively. In the present study, we used LPC treatment to induce various degrees of surface area loss and assessed several cellular changes: cell shape, S/V ratio, and cell deformability.…”

Theoretical model of reticulocyte to erythrocyte shape transformation

“…There are two general hypotheses regarding RBC shape (Nakao, 2002): the lipid bilayer coupled theory (Sheetz and Singer, 1974) and the protein network scaffold theory (Khodadad et al, 1996), recently combined to successfully describe the crenated, echinocytic shapes or the stomatocytediscocyte-echinocyte sequence resultant area-difference-elasticity model with spontaneous curvature and the membrane skeleton, ADE-SC-MS (Svetina et al, 1985;Helfrich, 1973;Evans and Skalak, 1980), which considers the membrane as a closed system, can be successfully applied in investigations of locally stable configurations of erythrocyte shape at fixed cell volume and neutral surface area, but at a varying area difference between the bilayer leaflets. The area difference is considered as deviating from its relaxed value, treated as a constant key parameter.…”