Leukocyte-platelet complexes in the pathogenesis of acute coronary syndrome. Part 2

Authors: Pinegina N.V.

Company: A.I. Evdokimov Moscow State University of Medicine and Dentistry of Ministry of Health of the Russian Federation; ulitsa Delegatskaya, 20, stroenie1, Moscow, 127473, Russian Federation

For correspondence:  Sign in or register.


DOI: https://doi.org/10.15275/kreatkard.2016.03.02

For citation: Pinegina N.V.. Leukocyte-platelet complexes in the pathogenesis of acute coronary syndrome. Part 2. Kreativnaya Kardiologiya. 2016; 10 (3): 201-209 (in Russian)

Keywords: acute coronary syndrome atherosclerosis leukocyte-platelet complexes extracellular vesicles flow cytometry

Full text:  

 

Abstract

Traditionally, the role of platelets in the pathogenesis of acute coronary syndrome (ACS), as suggested, is the thrombus formation at the site of an atherosclerotic plaque rupture. Formation of leukocyte-platelet complexes (LTC) can be a link between inflammation and thrombosis in the process of platelet activation in ACS. Although the increase in leukocyte aggregates with platelets in ACS was described earlier, the contribution of complex formation in the progression of atherosclerosis and plaque destabilization is unclear. It is also unknown whether the formation of LTC is a systemic phenomenon or plays a role in the pathogenesis of the local intracoronary inflammation in ACS. Also it is unclear whether leukocyte aggregates detected in peripheral blood are complexes with platelets or with platelet-derived extracellular vesicles. This review presents the mechanisms of formation of LTC, methods for determination of leukocyte-platelet aggregates in the peripheral blood, and the impact of treatment on the formation and stability of the LTC.

References

  1. Hargett L.A., Bauer N.N. On the origin of microparticles: From “platelet dust” to mediators of intercellular communication. Pulm. Circ. 2013; 3: 329–40.
  2. Morel O., Jesel L., Freyssinet J.M., Toti F. Cellular mechanisms underlying the formation of circulating microparticles. Arterioscler. Thromb. Vasc. Biol. 2011; 31: 15–26.
  3. Barteneva N.S., Fasler-Kan E., Bernimoulin M., Stern J.N., Ponomarev E.D., Duckett L. et al. Circulating microparticles: square the circle. BMC Cell. Biol. 2013; 14: 23.
  4. Vagida M., Grivel J.-C., Arakelyan A., Ryazankina N., Lebedeva A., Shpektor A. et al. Plateletderived extracellular vesicles in blood of patients with acute coronary syndrome. J. Extracell. Vesicles. 2015; 4: 126.
  5. Vagida M.S., Arakelyan A., Lebedeva A.M., Grivel J.-C., Shpektor A.V., Vasilieva E.Yu. et al. Analysis of extracellular vesicles using magnetic nanoparticles in blood of patients with acute coronary syndrome. Biochemistry. 2016; 81: 382–91.
  6. Feng B., Chen Y., Luo Y., Chen M., Li X., Ni Y. Circulating level of microparticles and their correlation with arterial elasticity and endothelium-dependent dilation in patients with type 2 diabetes mellitus. Atherosclerosis. 2010; 208: 264–9.
  7. Loyer X., Vion A.C., Tedgui A., Boulanger C.M. Microvesicles as cell-cell messengers in cardiovascular diseases. Circ. Res. 2014; 114: 345–53.
  8. Mause S.F., Von Hundelshausen P., Zernecke A., Koenen R.R., Weber C. Platelet microparticles: a transcellular delivery system for RANTES promoting monocyte recruitment on endothelium. Arterioscler. Thromb. Vasc. Biol. 2005; 25: 1512–8.
  9. Raposo G., Stoorvogel W. Extracellular vesicles: exosomes, microvesicles, and friends. J. Cell. Biol. 2013; 200: 373–83.
  10. Passacquale G., Vamadevan P., Pereira L., Hamid C., Corrigall V., Ferro A. Monocyte-platelet interaction induces a pro-inflammatory phenotype in circulating monocytes. PLoS One. 2011; 6: e25595.
  11. Forlow S.B., McEver R.P., Nollert M.U. Leukocyteleukocyte interactions mediated by platelet microparticles under flow. Blood. 2000; 95: 1317–23.
  12. Granja T., Schad J., Sch P., Fischer C., Helene H., Rosenberger P. et al. Using six-colour flow cytometry to analyse the activation and interaction of platelets and leukocytes – a new assay suitable for bench and bedside conditions. Thromb. Res. 2015; 136: 786–96.
  13. Xiao Z., Théroux P. Clopidogrel inhibits plateletleukocyte interactions and thrombin receptor agonist peptide-induced platelet activation in patients with an acute coronary syndrome. J. Am. Coll. Cardiol. 2004; 43: 1982–8.
  14. Box C.L., Yates C., Chimen M., Harrison M., Nash G., Watson S. et al. The formation of monocyte- platelet aggregates in stirred whole blood in response to different platelet agonists. Atherosclerosis. 2014; 232: 257–422, e1–e104.
  15. Gabbasov Z., Ivanova O., Kogan-Yasny V., Ryzhkova E., Saburova O., Vorobyeva I. et al. Activated platelet chemiluminescence and presence of CD45+ platelets in patients with acute myocardial infarction. Platelets. 2014; 25: 405–8.
  16. Brambilla M., Camera M., Colnago D., Marenzi G., De Metrio M., Giesen P.L. et al. Tissue factor in patients with acute coronary syndromes: expression in platelets, leukocytes, and platelet-leukocyte aggregates. Arterioscler. Thromb. Vasc. Biol. 2008; 28: 947–53.
  17. O/ sterud B., Olsen J.O. Human platelets do not express tissue factor. Thromb. Res. 2013; 132: 112–5.
  18. Del Conde I., Shrimpton C.N., Thiagarajan P., Lo A. Tissue-factor – bearing microvesicles arise from lipid rafts and fuse with activated platelets to initiate coagulation. Blood. 2005; 106: 1604–11.
  19. Scholz T., Temmler U., Krause S., Heptinstall S., Lösche W. Transfer of Tissue Factor from Platelets to Monocytes: Role of Platelet-Derived Microvesicles and CD62P. Thromb. Haemost. 2002; 88: 1033–9.
  20. Sims P.J., Wiedmer T., Esmon C.T., Weiss H.J., Shattil S.J. Assembly of the platelet prothrombinase complex is linked to vesiculation of the platelet plasma membrane. studies in scott syndrome: an isolated defect in platelet procoagulant activity. J. Biol. Chem. 1989; 264: 17049–57.
  21. Ott I., Neumann F.-J., Gawaz M., Schmitt M., Schomig A. Increased neutrophil-platelet adhesion in patients with unstable angina. Circulation. 1996; 94: 1239–46.
  22. Furman M.I., Barnard M.R., Krueger L.A., Fox M.L., Shilale E.A., Lessard D.M. et al. Circulating monocyte-platelet aggregates are an early marker of acute myocardial infarction. J. Am. Coll. Cardiol. 2001; 38: 1002–6.
  23. Furman M.I., Benoit S.E., Barnard M.R., Valeri C.R., Borbone M.L., Becker R.C. et al. Increased platelet reactivity and circulating monocyte-platelet aggregates in patients with stable coronary artery disease. J. Am. Coll. Cardiol. 1998; 31: 352–8.
  24. Mickelson J.K., Lakkis N.M., Villarreal-Levy G., Hughes B.J., Smith C.W. Leukocyte activation with platelet adhesion after coronary angioplasty: a mechanism for recurrent disease? J. Am. Coll. Cardiol. 1996; 28: 345–53.
  25. Aurigemma C., Scalone G., Fattorossi A., Sestito A., Lanza G.A., Crea F. Adenosine inhibition of adenosine diphosphate and thrombininduced monocyte-platelet aggregates in cardiac syndrome X. Thromb. Res. 2009; 24: 116–20.
  26. Neumann F.J., Zohlnhöfer D., Fakhoury L., Ott I., Gawaz M., Schömig A. Effect of glycoprotein IIb/IIIa receptor blockade on platelet-leukocyte interaction and surface expression of the leukocyte integrin Mac-1 in acute myocardial infarction. J. Am. Coll. Cardiol. 1999; 34: 1420–6.
  27. Mccabe D.J.H., Harrison P., Mackie I.J., Sidhu P.S., Lawrie A.S., Watt H. et al. Platelet degranulation and monocyte – platelet complex formation are increased in the acute and convalescent phases after ischaemic stroke or transient ischaemic attack. Br. J. Haematol. 2004; 125: 777–87.
  28. Klinkhardt U., Bauersachs R., Adams J., Graff J. Clopidogrel but not aspirin reduces P-selectin expression and formation of platelet-leukocyte aggregates in patients with atherosclerotic vascular disease. Clin. Pharmacol. Ther. 2003; 73: 232–41.
  29. Graff J., Harder S., Wahl O., Scheuermann E.-H., Gossmann J. Anti-inflammatory effects of clopidogrel intake in renal transplant patients: effects on platelet-leukocyte interactions, platelet CD40 ligand expression, and proinflammatory biomarkers. Clin. Pharmacol. Ther. 2005; 78: 468–76.
  30. Harding S.A., Sarma J., Din J.N., Maciocia P.M., Newby D.E., Fox K.A.A. Clopidogrel reduces platelet-leucocyte aggregation, monocyte activation and RANTES secretion in type 2 diabetes mellitus. Heart. 2006; 92: 1335–7.
  31. Tuttle H.A., Davis-Gorman G., Goldman S., Copeland J.G., Mcdonagh P.F. Platelet-neutrophil conjugate formation is increased in diabetic women with cardiovascular disease. Cardiovasc. Diabetol. 2003; 2: 1–16.
  32. Sener A., Ozsavci D., Oba R., Demirel G.Y., Uras F., Yardimci K.T. Do platelet apoptosis, activation, aggregation, lipid peroxidation and plateletleukocyte aggregate formation occur simultaneously in hyperlipidemia? Clin. Biochem. 2005; 38: 1081–7.
  33. Wang Y., Li Z., Wang W. Platelet-leukocyte interaction in atherosclerosis and atherothrombosis: what we have learnt from human studies and animal models. J. Cardiol. Ther. 2014; 1: 92–7.
  34. Wang J., Zhang S., Jin Y., Qin G., Yu L., Zhang J. Elevated levels of platelet – monocyte aggregates and related circulating biomarkers in patients with acute coronary syndrome. Int. J. Cardiol. 2007; 115: 361–5.
  35. Czepluch F.S., Kuschicke H., Dellas C., Riggert J., Hasenfuss G., Sch K. Increased proatherogenic monocyte – platelet cross-talk in monocyte subpopulations of patients with stable coronary artery disease. J. Intern. Med. 2014; 275: 144–54.
  36. Lukasik M., Dworacki G., Kufel-Grabowska J., Watala C., Kozubski W. Upregulation of CD40 ligand and enhanced monocyte-platelet aggregate formation are associated with worse clinical outcome after ischaemic stroke. Thromb. Haemost. 2012; 107: 346–55.
  37. Mccabe D.J.H., Harrison P., Mackie I.J., Sidhu P.S., Purdy G., Lawrie A.S. et al. Increased platelet count and leucocyte–platelet complex formation in acute symptomatic compared with asymptomatic severe carotid stenosis. J. Neurol. Neurosurg. Psychiatry. 2005; 76: 1249–54.
  38. Schrottmaier W.C., Kral J.B., Badrnya S., Assinger A. Aspirin and P2Y12 inhibitors in plateletmediated activation of neutrophils and monocytes. Thromb. Haemost. 2015; 114: 478–89.
  39. Nagy B., Jr, Kerényi A., Clemetson K.J., Kappelmayer J. Potential Therapeutic Targeting of Platelet- Mediated Cellular Interactions in Atherosclerosis and Inflammation. Curr. Med. Chem. 2012; 19: 518–31.
  40. Rainger G.E., Chimen M., Harrison M.J., Yates C.M., Harrison P., Watson S.P. et al. The role of platelets in the recruitment of leukocytes during vascular disease. Platelets. 2015; 26: 507–20.
  41. Scholz T., Zhao L., Temmler U., Bath P., Heptinstall S., Wolfgang L. The GPIIb / IIIa antagonist eptifibatide markedly potentiates platelet – leukocyte interaction and tissue factor expression following platelet activation in whole blood in vitro. Platelets. 2002; 13: 401–6.
  42. Barnard M.R., Linden M.D., Frelinger A.L., Li Y., Fox M.L., Furman M.I. et al. Effects of platelet binding on whole blood flow cytometry assays of monocyte and neutrophil procoagulant activity. J. Thromb. Haemost. 2005; 3: 2563–70.
  43. Barr J., Barr J., Meurice M., Motto D. Scanning Electron Microscopy Study of Endothelial Injury and Thrombus Formation in WT and VWF Deficient Mice. Blood. 2009; 114: 3062.
  44. Bournazos S., Rennie J., Hart S.P., Fox K.A.A., Dransfield I. Monocyte functional responsiveness after PSGL-1-mediated platelet adhesion is dependent on platelet activation status. Arterioscler. Thromb. Vasc. Biol. 2008; 28: 1491–8.
  45. Harding S.A., Din J.N., Sarma J., Jessop A., Weatherall M., Fox K.A.A. et al. Flow cytometric analysis of circulating platelet-monocyte aggregates in whole blood: Methodological considerations. Thromb. Haemost. 2007; 98: 451–6.
  46. Majumder B., North J., Mavroudis C., Rakhit R., Lowdell M.W. Improved accuracy and reproducibility of enumeration of platelet – monocyte complexes through use of doublet-discriminator strategy. Cytometry Part B. 2012; 82 (6): 353–9.

Chief Editor

Leo A. Bockeria, MD, PhD, DSc, Professor, Academician of Russian Academy of Sciences, President of Bakoulev National Medical Research Center for Cardiovascular Surgery