Red cells slide as they form doublets and deform in rouleaux

Mammalian erythrocyte aggregation increases when the levels of plasma proteins favoring aggregation rise. Red cell aggregate formation has been attributed to noncovalent bonding of adjacent erythrocyte plasma membranes by these proteins and similar macromolecules. The proposed membrane to membrane noncovalent bonds would keep each membrane from sliding during aggregate formation because the bonds responsible for maintaining cell-cell contact would need to be disrupted. Because past studies of doublet formation suggested that the membranes might slide during contact expansion, we embedded latex particles in the membranes of individual human red cells and recorded doublet formation on video tape. The cells were suspended in a buffer that contained polyvinylpyrrolidone at a concentration sufficient to cause a moderately elevated sedimentation rate. The latex particles remained stable in position relative to each host cell during doublet formation, indicating that sliding was involved. We also stretched individual rouleaux using a glass rod and observed that latex particles attached to red cells whose contact area was reduced by the motion maintained their position during their return to a normal shape. These studies show that erythrocyte aggregate formation is accomplished by membrane sliding and that aggregate shape change and disruption during blood flow commonly involve sliding. The sliding motion argues that the attraction between red cell membranes generated by an array of elongated macromolecules involves a delocalized rather than a noncovalently coordinated adhesion.