Cell-surface dynamics, platelet

Red cell-surface interactions may play a major role in the dynamics of protein and platelet behaviour at the interface. The effect of red cells on platelet sticking has been noted widely, causing an augmentation of the rate of adhesion, probably by a combination of physical and biochemical mechanisms (40). Hellem et al (45) have observed that red cell ghosts restore retension of platelets in colunrn almost as... 

Hyaluronic acid into PU Bulk modification Bulk versus surface modification Platelet response, cell proliferation Dynamic, in vitro Human PRP, endothelial cells Hyaluronic acid stable in bulk modified PU, better antiplatelet properties, good cell proliferation [96]... 

Ruckenstein, E., A. Marmur and S. R. Rakower. 1976. Sedimentation and Adhesion of Platelets from Platelet Rich Plasma onto Glass Surface. submitted for publication. Ruekenstein, E. and D. C. Prieve. 1975. Dynamics of Cell Deposition on Surfaces. J. Theor. Biol., 51, 429-438. 

The work discussed here has shown that suspensions of platelets and red cells in a physiological medium can provide information for platelet surface interactions. Evidence is provided on the dynamic features of platelet-surface adhesion and detachment which indicates that more than one sequence of adhesion, detachment and re-adhesion can lead to the same net platelet adhesion. Surface generated substances, such as A DP and serotonin from platelets and thrombin from the coagulation pathway, may strongly influence the function of platelets approaching a surface. The supply of these substances depends on the presence of flow and continued arrival of platelets at a surface. The reactivity of surface-bound protein may be altered by platelet adhesion and detachment. This may occur as a result of deposition of cell membrane components, replacement of the original substrate with protein secreted from platelets or possibly by enzymatic digestion of surface bound protein. 

The first component is that of the protein adsorption mentioned above. This process is initiated as soon as a material comes into contact with tissue fluids such that relatively quickly the surface of the biomaterial is covered with a layer of protein. The kinetics and extent of this process will vary from material to material which will in any case be a dynamic phenomenon with adsorption and desorption processes continuously taking place. Under some circumstances, this layer is extremely important in controlling the development of the host response since cell behavior near the material may depend on interactions with these proteins. For example, thrombogenicity is controlled by a number of events including the interaction between plasma proteins and surfaces, these proteins being able to influence the attachment of platelets to the surface. In other circumstances, the effects of this protein layer are far from clear. 

The majority of hemocompatibility studies are performed under static conditions, but some groups considered the effect of flow on platelet adhesion in dynamic experiments. As one example, randomly structured PMMA surfaces with feature sizes of 40 nm, 80 nm, and 400 nm and heights of 3nm, 13 nm, and 50 nm were investigated under flow conditions [108,109], Experiments with human whole blood showed a preferred adsorption of vWF compared to that of fibrinogen and albumin, which is in conflict with other static studies. It is apparent that different adsorption behaviors of plasma proteins can be observed under different flow conditions. The platelet adhesion was highest on those samples with the most vWF adhesion, namely the larger structures. Experiments were carried out with washed platelets and revealed other results. Platelets preferred the smaller structured surfaces for adhesion, which shows the severe influence of blood cells and plasma proteins on the adhesion behavior of platelets [108]. 

On the basis of a concentration of 2.4 x 10 molecules of sialic acid per cell, a high sialyltransferase activity, and a measurable neuraminidase activity at the surface of the human blood platelet, Bosmann (1972) proposed that platelet aggregation could result from an interaction, at the surface of the cell, between the sialyltransferases and the galactosyl residues liberated by the action of the neuraminidase. This application of Roseman s (1970) theory to platelet aggregation would require a dynamic equilibrium of transfers and removals of sialic acid residues, with continuous formation, degradation, and reformation of the enzyme-substrate complexes. 

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