Effects of C-reactive protein on platelet function. I. Inhibition of platelet aggregation and release reactions.
C-reactive protein (CRP) is an acute phase reactant which shares numerous functional characteristics with the immunoglobulins. In the present study CRP was found to inhibit the aggregation of human platelets stimulated by either modified human immunoglobulin or thrombin. This effect did not involve chelation of calcium or cytotoxicity, and was overcome by larger amounts of the aggregating agents. CRP also inhibited the activation but not the activity of platelet factor 3 and the release of beta-glucuronidase. Thus, CRP can inhibit multiple platelet  reactivities. We suggest that this property of CRP may play an important role in the control of platelet responsiveness during reactions of inflammation, defense, and repair.
D001792:Blood Platelets / Q000502:physiology*; D002097:C-Reactive Protein / Q000494:pharmacology*; D002470:Cell Survival / Q000187:drug effects; D005966:Glucuronidase / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D010974:Platelet Aggregation / Q000187:drug effects*; D010977:Platelet Factor 3 / Q000378:metabolism; D013917:Thrombin / Q000494:pharmacology; D005719:gamma-Globulins / Q000494:pharmacology
D005719:gamma-Globulins; D010977:Platelet Factor 3; D002097:C-Reactive Protein; D005966:Glucuronidase; D013917:Thrombin