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We previously reported that C-reactive protein bioactivity on thrombogenesis was based on loss of its pentameric symmetry, resulting in formation of monomeric C-reactive protein. Our purpose was to provide mechanistic information on the direct effects of C-reactive protein isoforms on platelet activation and provide a C-reactive protein dissociation mechanism in circulating blood.

Monomeric C-reactive protein is prothrombotic and dissociates from circulating pentameric C-reactive protein on adhered activated platelets under flow