Abstract

Four different dynamic biomaterial surfaces with different molecular architectures were prepared using two hydrophilic polymers: poly(ethylene glycol) and polyrotaxanes containing α-cyclodextrin. Either one or both terminals of the poly(ethylene glycol) or polyrotaxanes were immobilized onto a gold substrate via Au-S bonds, resulting in poly(ethylene glycol)-graft, polyrotaxanes-graft, poly(ethylene glycol)-loop, and polyrotaxanes-loop structures. Human platelet adhesion was suppressed more effectively on the graft surfaces than on the loop surfaces for both poly(ethylene glycol) and polyrotaxanes due to the high mobility of graft polymer chains with a free terminal. Moreover, the platelets adhered to the polyrotaxane surfaces much less than the poly(ethylene glycol) surfaces, possibly because of the mobile nature of the α-cyclodextrin molecules that were threaded on the poly(ethylene glycol) chain. Actin filament assembly in adherent platelets was also greatly prevented on the poly(ethylene glycol)/polyrotaxanes-graft surfaces in comparison with the corresponding loop surfaces. A clear correlation between the numbers and areas of adherent platelets on these surfaces suggests that platelet adhesion and activation were dominated by the platelet GPIIb/IIIa-adsorbed fibrinogen interaction. These results indicate that both of the different modes of dynamic features, sliding/rotation of α-cyclodextrin and polymer chain mobility, effectively suppressed platelet adhesion in spite of the similar hydrophilicity. This research affords a novel chemical strategy for designing hemocompatible biomaterial surfaces.

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