Thromb Haemost 2014; 111(06): 1184-1186
DOI: 10.1160/TH13-08-0704
Letters to the Editor
Schattauer GmbH

Phosphatidylserine exposure, microparticle formation and mitochondrial depolarisation in Glanzmann thrombasthenia platelets

Hong Wang
1   Physiology and Experimental Medicine Program, Research Institute, The Hospital for Sick Children, Toronto, Canada
,
K. W. Annie Bang
2   Lunenfeld-Tanenbaum Research Institute, Mount Sinai Hospital, Toronto, Canada
,
Victor S. Blanchette
3   Division of Haematology/ Oncology, The Hospital for Sick Children, Toronto, Canada
4   Department of Paediatrics, University of Toronto, Canada
,
Alan T. Nurden
5   Plateforme Technologique et d’Innovation Biomédicale, Hôpital Xavier Arnozan, Pessac, France
,
Margaret L. Rand
1   Physiology and Experimental Medicine Program, Research Institute, The Hospital for Sick Children, Toronto, Canada
3   Division of Haematology/ Oncology, The Hospital for Sick Children, Toronto, Canada
6   Department of Laboratory Medicine and Pathobiology, University of Toronto, Canada
› Institutsangaben
Financial support: This work was supported by grant #107 from the Heart and Stroke Foundation of Ontario.
Weitere Informationen

Publikationsverlauf

Received: 26. August 2013

Accepted after major revision: 03. Januar 2014

Publikationsdatum:
02. Dezember 2017 (online)

 

 
  • References

  • 1 Nurden AT, Pillois X, Nurden P. Understanding the genetic basis of Glanzmann thrombasthenia: implications for treatment. Expert Rev Hematol 2012; 05: 487-503.
  • 2 Reverter JC, Beguin S, Kessels H. et al. Inhibition of platelet-mediated, tissue factor-induced thrombin generation by the mouse/human chimeric 7E3 antibody. Potential implications for the effect of c7E3 Fab treatment on acute thrombosis and “clinical restenosis”. J Clin Invest 1996; 98: 863-874.
  • 3 Beguin S, Kumar R, Keularts I. et al. Fibrin-dependent platelet procoagulant activity requires GPIb receptors and von Willebrand factor. Blood 1999; 93: 564-570.
  • 4 Dargaud Y, Bordet JC, Trzeciak MC. et al. A case of Glanzmann's thrombasthenia successfully treated with recombinant factor viia during a surgical procedure: observations on the monitoring and the mechanism of action of this drug. Haematologica 2006; 91: 17-20.
  • 5 Keuren JF, Ulrichts H, Feijge MA. et al. Integrin alphaIIbbeta3 and shear-dependent action of glycoprotein Ibalpha stimulate platelet-dependent thrombin formation in stirred plasma. J Lab Clin Med 2003; 141: 350-358.
  • 6 Bevers EM, Comfurius P, Nieuwenhuis HK. et al. Platelet prothrombin converting activity in hereditary disorders of platelet function. Br J Haematol 1986; 63: 335-345.
  • 7 Weiss HJ, Lages B. Platelet prothrombinase activity and intracellular calcium responses in patients with storage pool deficiency, glycoprotein IIb-IIIa deficiency, or impaired platelet coagulant activity--a comparison with Scott syndrome. Blood 1997; 89: 1599-1611.
  • 8 Gemmell CH, Sefton MV, Yeo EL. Platelet-derived microparticle formation involves glycoprotein IIb-IIIa. Inhibition by RGDS and a Glanzmann's thrombasthenia defect. J Biol Chem 1993; 268: 14586-14589.
  • 9 Holme PA, Solum NO, Brosstad F. et al. Stimulated Glanzmann's thrombasthenia platelets produced microvesicles. Microvesiculation correlates better to exposure of procoagulant surface than to activation of GPIIb-IIIa. Thromb Haemost 1995; 74: 1533-1540.
  • 10 van der Meijden PE, Feijge MA, Swieringa F. et al. Key role of integrin alpha(IIb)beta (3) signaling to Syk kinase in tissue factor-induced thrombin generation. Cell Mol Life Sci 2012; 69: 3481-3492.
  • 11 Weiss HJ. Impaired platelet procoagulant mechanisms in patients with bleeding disorders. Semin Thromb Hemost 2009; 35: 233-241.
  • 12 Lages B, Weiss HJ. Greater inhibition of platelet procoagulant activity by antibody-derived glycoprotein IIb--IIIa inhibitors than by peptide and peptidomimetic inhibitors. Br J Haematol 2001; 113: 65-71.
  • 13 Goto S, Tamura N, Li M. et al. Different effects of various anti-GPIIb-IIIa agents on shear-induced platelet activation and expression of procoagulant activity. J Thromb Haemost 2003; 01: 2022-2030.
  • 14 Rand ML, Wang H, Bang KW. et al. Phosphatidylserine exposure and other apoptotic-like events in Bernard-Soulier syndrome platelets. Am J Hematol 2010; 85: 584-592.
  • 15 Shadle PJ, Ginsberg MH, Plow E F. et al. Platelet-collagen adhesion: inhibition by a monoclonal antibody that binds glycoprotein IIb. J Cell Biol 1984; 99: 2056-2060.
  • 16 Heemskerk JW, Mattheij NJ, Cosemans JM. Platelet-based coagulation: different populations, different functions. J Thromb Haemost 2013; 11: 2-16.
  • 17 Rand ML, Wang H, Bang KW. et al. Procoagulant surface exposure and apoptosis in rabbit platelets: association with shortened survival and steady-state senescence. J Thromb Haemost 2004; 02: 651-659.
  • 18 Leung R, Gwozdz AM, Wang H. et al. Persistence of procoagulant surface expression on activated human platelets: involvement of apoptosis and aminophospholipid translocase activity. J Thromb Haemost 2007; 05: 560-570.
  • 19 Gwozdz AM, Leung R, Wang H. et al. Calpain inhibition by calpeptin does not prevent APLT activity reduction in PS-exposing platelets, but calpeptin has independent pro-apoptotic effects. Thromb Haemost 2010; 103: 1218-1227.
  • 20 van Kruchten R, Mattheij NJ, Saunders C. et al. Both TMEM16F-dependent and TMEM16F-independent pathways contribute to phosphatidylserine exposure in platelet apoptosis and platelet activation. Blood 2013; 121: 1850-1857.
  • 21 Lhermusier T, Chap H, Payrastre B. Platelet membrane phospholipid asymmetry: from the characterisation of a scramblase activity to the identification of an essential protein mutated in Scott syndrome. J Thromb Haemost 2011; 09: 1883-1891.