Interactions

Cellular interactions between platelets and vascular endothelium or other blood cellular components regulate the hemostatic process. Platelets can even interact and play a role in the activity of pathologic elements such as tumor cells or infectious agents. Moreover, it has been described that platelet interactions can interfere with the effectiveness of antiplatelet drugs.

  • Vascular endothelium: The endothelium does not form a passive barrier for blood circulation. Endothelial cells and several of their active metabolites, including eicosanoids such as prostacyclin (PGI2) and endothelial-derived relaxing factor (nitric oxide), are known to directly influence platelet reactivity.
  • Leukocytes: The activating and inhibitory mechanisms triggered by the interactions between platelets and leukocytes are widely recognized. Lipoxygenase products such as HETEs and several surface glycoproteins play a role in platelet-leukocyte cross-talk, which is favored by pathophysiologic events at sites of inflammation, thrombosis and vascular injury.
  • Erythrocytes: Red blood cells play an important role in modulating platelet reactivity with subendothelial structures, mainly through rheological mechanisms (i.e., erythrocyte deformability and erythrocyte aggregation), although the influence of red cell metabolites on platelet functions is also important.
  • Tumoral cells: Platelet ability to interact with tumor cells is involved in the success of metastatic spread. Moreover, thrombotic events are often associated with cancer due to the capacity of tumor cells to produce and secrete procoagulant/fibrinolytic substances and inflammatory cytokines.
  • Infectious agents: Platelet binding by bacterial pathogens is thought to facilitate the establishment of certain infections. Furthermore, association of virus with platelets may represent a viral transfer and a passive vehicle for viral dissemination.

Left: endothelial cells in culture (micrograph by M. Diaz-Ricart); middle:platelet-leukocyte heterotypical aggregation (micrograph by M.R. Hernández) ; Right: platelet and leukocyte interaction with a tumor cell (micrograph by A. Ordinas). Click on pictures to enlarge. (For image uses, please see Use of Content at Legal Information).

Bibliography

Baumgartner HR, Haudenschild C. Adhesion of platelets to subendothelium. Ann N Y Acad Sci. 1972; 201: 22-36. 10.1111/j.1749-6632.1972.tb16285.x.

Weiss HJ, Turitto VT, Baumgartner HR. Platelet adhesion and thrombus formation on subendothelium in platelets deficient in glycoproteins IIb-IIIa, Ib, and storage granules. Blood. 1986; 67: 322-30.

Bastida E, Escolar G, Almirall L, Ordinas A. Platelet activation induced by a human neuroblastoma tumor cell line is reduced by prior administration of ticlopidine. Thromb Haemost. 1986; 55: 333-7.

Escolar G, Garrido M, Mazzara R, Castillo R, Ordinas A. Experimental basis for the use of red cell transfusion in the management of anemic-thrombocytopenic patients. Transfusion. 1988; 28: 406-11. 10.1046/j.1537-2995.1988.28588337325.x.

Arderiu G, Diaz-Ricart M, Buckley B, Escolar G, Ordinas A. Primary arrest of circulating platelets on collagen involves phosphorylation of Syk, cortactin and focal adhesion kinase: studies under flow conditions. Biochem J. 2002; 364: 65-71. 10.1042/bj3640065.

Escolar G, Lopez-Vilchez I, Diaz-Ricart M, White JG, Galan AM. Internalization of tissue factor by platelets. Thromb Res. 2008; 122 Suppl 1: S37-41. 10.1016/S0049-3848(08)70017-3.