ISSN: 2469-2778 HTIJ

Hematology & Transfusion International Journal
Volume 1 Issue 1 - 2015
Platelets: Are They Only an “Hemostatic Player”?
Anna Komitopoulou*
1Oregon Health Sciences Center, USA
2Kaiser Medical Group, USA
Received: January 21, 2015 | Published: January 28, 2015
*Corresponding author: Anna Komitopoulou, Consultant Hematologist, Hygei” Hospital, 6 Parnassou str, Maroussi, 15124, Athens, Greece, Email:
Citation: Komitopoulou A (2014) Platelets: Are They Only an “Hemostatic Player”?. Hematology & Transfusion International Journal 1(1): 00002. DOI: 10.15406/htij.2015.01.00002


Platelets are small (5-9 fl) blood cells, with discoid structure (1.5μm x 0.5-1μm), without nucleous. They are derived from megakaryocytes and enter in the circulation while being under the regulation of thrombopoeitin, a hormone produced mainly in the liver. Platelets are found in mammals, probably as an evaluating process after severe bleeding. They are constituted of many glycoprotein receptors and proteins (such as GPIb/IX/V, GPIb/IIa, GPVI, PAR1, PAR2, P2Y12, P-selectin), all of which are related to platelets adhesion and aggregation and of many platelet organelles as dense and a-granules which include substances related to clot formation, induction signaling of endothelial cells and control of haemostasis in general [1-4].

While the significant role of platelets in the haemostatic process is certain, information about their role in the inflammatory process is gaining attention recently. Specifically, platelets interact with Gram positive or Gram negative bacteria and defense against them through platelet microbicidal proteins (PMPs), which are small cationic proteins of the antimicrobial armamentarium and kinocidins, which are chemokines with direct and indirect microbicidal activities. Interaction has been described also with Neutrophils, monocytes and lymphocytes. Constituents of a-granules like PF4 (platelet factor 4) or SDF-1 (stromal cell-derived factor 1), are chemokines that help the activation of immune cells whereas constituents of dense granules like ADP, polyphosphates, or serotonin have immune modifying effects implicating monocyte differentiation and enhancement of T-cell activation [5-9].

Additionally, acute phase response is modified by platelets, mainly via IL-1b (interleukin 1b) and binding to pathogens is induced by the expression of Toll-like receptors on platelets. Expression of TLR4 and TLR2 are the main receptors contributing to the interaction of platelets with neutrophil. Binding to neutrophils leads to the release of other chemokines and as a consequence the formation of neutrophil extracellular traps (NETS) which kill pathogens [8,10-13].

Platelets are also the major source of soluble CD40L, a “key” molecule of the adaptive immune response and B-cell immunoglobulin iso type switching. Modulation of dendritic cells (DC) through interactions between DC derived CD11b/CD18, T-cell enhancers and platelets have been documented [6,7,14,15]. Platelets also interact with the blood vessel endothelium, reinforce intercellular communication and spread the diverse repertoire of miRNAs that they carry, which are responsible for the vascular inflammation. Perhaps this could also interpret the interference of platelets in tumor growth and metastasis [16].

In addition, quite recently it has been found that platelets possess mRNA, whose expression plays a crucial role in cytokines and lipid mediators. Signaling of platelet aggregation through calcium channels in patients with diabetes mellitus and metabolic syndrome has been described [17-19]. We understand that until 130 years ago, platelets were thought to be just “dust” in the vessels, contributing only to haemostasis. Nowadays, special functions, especially that regarding inflammatory process modulation, are attributed to platelets. Expert research in this promising field, will probably give us more surprising results in the future.


  1. Schmaier AA, Stalker TJ, Runge JJ, Lee D, Nagaswami C, et al. (2011) Occlusive thrombi arise in mammals but not birds in response to arterial injury: evolutionary insight into human cardiovascular disease. Blood 118(13): 3661-3669.
  2. Nathan, Oski’s (2008) Hematology in infancy and childhood. (7th edn) Elsevier, USA, pp. 1872.
  3. Watson SP, Harrison P (2010) The vascular function of platelets. In: Hoffbrand AV et al. (Eds.), Postgraduate Haematology. (6th edn), Wiley-Blackwell, USA, pp.1074.
  4. Handin RI (2011) Blood platelets and the vessel wall. In: Colman RW et al. (Eds.), Thrombosis and Haemostasis Basic principles and Clinical Practice. (4th Edn), Lippincot Williams and Wilkins, pp.1451-1469.
  5. Yeaman MR (2010) Platelets in defense against bacterial pathogens. Cell Mol Life Sci 67(4): 525-544.
  6. Weyrich S, Andrew (2014) Platelets: more than a sack of glue. American society of hematology 2014(1): 400-403.
  7. Craig NM, Angela AA, Lesley MC, Kristina LM (2014) Emerging roles for platelets as immune and inflammatory cells. Blood 123(18): 2759-2767.
  8. Hidari KI, Weyrich AS, Zimmerman GA, McEver RP (1997) Engagement of P-selectin glycoprotein ligand-1 ehnances tyrosine phosphorylation and activates mitogen-activated protein kinases in human neutrophils. J Biol Chem 272(45): 28750-28756.
  9. Weyrich AS, Elstad MR, McEver RP, McIntyre TM, Moore KL, et al. (1996) Activated platelets signal chemokine synthesis by human monocytes. J Clin Invest 97(6): 1525-1534.
  10. Clark SR, Ma AC, Tavener SA, McDonald B, Goodarzi Z, et al. (2007) Platelet TLR4 activates neutrophil extracellular traps to ensare bacteria in septic blood. Nat Med 13(4): 463-469.
  11. Brickmann V, Zychlinsky A (2012) Neutrophil extracellular traps is immunity the second function of chromatin. J Cell Biol 198(5): 773-783.
  12. Lindenmann S, Tolley ND, Dixon DA, Thomas M. McIntyre, Stephen M. Prescott, et al. (2001) Activated platelets mediate inflammatory signaling by regulated interleukin 1beta synthesis. J Cell Biol 154(3): 485-490.
  13. Aslam R, Speck ER, Kim M, Crow AR, Bang kw, et al. (2006) Platelet Toll like receptor expression modulates lipopolysaccharide-induced thrombocytopenia and tumor necrosis factor-alpha production in vivo. Blood 107(2): 637-641.
  14. Sprague DL, Elzey BD, Crist SA, Waldschmidt TJ, Jensen RJ, et al. (2008) Platelet-mediated modulation of adaptive immunity:unique delivery of CD154 signal by platelet-derived membrane vesicles. Blood 111(10): 5028-5036.
  15. Langer HF, Daub K, Braun G, Schonberger T, May AE, et al. (2007) Platelets recruits human dendritic cells via Mac1/JAM-C interaction and modulate dendritic cell function in vitro. Atheroscler Thromb Vasc Biol 27(6): 1463-1470.
  16. Ple H, Landry P, Benham A, Coarfa C, Gunarante PH, et al. (2012) The repertoire and features of human platelet microRNAs. PLoS One 7(12): e50746.
  17. Denis MM, Tolley ND, Bunting M, Schwertz H, Jiang H, et al. (2005) Escaping the nuclear confines:signal dependent pre-mRNA splicing in anucleate platelets. Cell 122(3): 379-391.
  18. Rowley JW, Oler AJ, Tolley ND, Hunter BN, Low EN, et al. (2011) Genome-wide-RNA-seq analysis of human and mouse platelet trancriptomes. Blood 118(14): e101-e111.
  19. Borst O, Schmidt EM, Munzer P, Schonberger T, Towhid ST, et al. (2012) The serum-and glucorticosteroid-iducible kinase 1 (SGK 1) influences platelet calcium signaling and function by regulation of oral 1 expression in megakaryocytes. Blood 119(1): 251-261.
© 2014-2018 MedCrave Group, All rights reserved. No part of this content may be reproduced or transmitted in any form or by any means as per the standard guidelines of fair use.
Creative Commons License Open Access by MedCrave Group is licensed under a Creative Commons Attribution 4.0 International License.
Based on a work at
Best viewed in Mozilla Firefox | Google Chrome | Above IE 7.0 version | Opera |Privacy Policy