R&D Systems supports platelet research with a full line of recombinant proteins, antibodies, and assays. Our immunoassay selection includes Quantikine® and DuoSet® ELISA kits, ELISpot kits, Luminex® Assays, Proteome Profiler™ Antibody Arrays, and Simple Plex™ automated assays. Our sister brand Tocris Bioscience supplies a wide range of small molecule agonists, antagonists and enzyme inhibitors for the study of platelets and coagulation. We also provide stem cell and cell culture products to support your research. Learn More.
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Recombinant Proteins
Quantikine® and DuoSet® ELISA Kits
Small Molecule Agonists and Antagonists
Platelet Literature and Resources
Brochures and Product Guides
Cardiovascular Research Product Guide
Products for Chemokine Research
Products for Glycobiology Research
Products for Angiogenesis Research
Posters
References and Troubleshooting Guides
Blood Coagulation Signaling Pathways
Atherosclerosis Disease Progression Cell Markers
Chemokine Superfamily Pathway: Human/Mouse Ligand-Receptor Interactions
Protocols/Troubleshooting Guides From Novus Biologicals
Protocols/Troubleshooting Guides From R&D Systems®
Background
Platelets are non-nucleated cells that function as critical mediators of coagulation, hemostasis, and inflammation. Circulating platelets can be activated by many soluble ligands including ADP, Thrombin, 5-HT/serotonin, and Thromboxane A2. GP family glycoproteins and activated Integrins mediate platelet adhesion to the vascular endothelium at sites of damage to the vessel wall. During a very rapid burst of activation, platelets release intracellular granules which deliver regulators of coagulation (both positive and negative), inflammation, and wound healing. Granule contents also trigger platelet aggregation into fibrin networks to plug damaged vessels and halt bleeding.
Platelets are normally maintained in an inactive state by multiple factors such as nitric oxide and PGI2/prostacyclin derived from healthy endothelial cells. Pathological activation of platelets is a serious complication of many diseases including atherosclerosis, stroke, deep vein thrombosis, and pulmonary thromboembolism. Pharmacological control of dangerous clot formation can be addressed with anticoagulants/blood thinners (e.g. aspirin or thienopyridines) or thrombolytics/clot dissolving drugs (e.g. tPA or uPA). There is a delicate balance between pathological thrombosis and risk of increased bleeding.