Adhesion molecule jam-a and hemostasis at women with hypertensive disease: 616-053:616.15
Тромбоз, гемостаз и реология

Tromboz, Gemostaz I Reologiya
scientific and practical journal

ISSN 2078–1008 (Print); ISSN 2687-1483 (online)
Тромбоз, гемостаз и реология. — 2017. — №3(71)

Keywords

adhesion molecule JAM-A
hemostasis
plasma clotting factors
rate of fibrin clot formation
platelet
monocyte
endothelial microvesicles

Abstract

Introduction. Adhesion is a complex of physiological reactions. Junctional adhesion molecule-A (JAM-A) is a specific molecule that regulates permeability of endothelium and epithelium, migration of leukocytes during inflammation. Recently it was shown that JAM-A can be involved in pathogenesis of hypertension and hypertensive crises.

The aim was to study the relationship between the blood level of adhesion molecule JAM-A and hemostasis.

Materials and methods. We examined 37 women aged 57,8{±{5,7 years old with arterial hypertension stage II. The control group consisted of 30 relatively healthy women, comparable in age and body weight. The following parameters were examined: blood clotting time, platelet count, activated partial thromboplastin time, prothrombin time with calculation of INR, thrombin time, plasma factors IIa, IX, X, Xa content, fibrinogen level, concentration of soluble fibrin-monomer complexes and D-dimers, activity of antithrombin III and protein C, XIIa-dependent fibrinolysis. Also we examined extensional growth of fibrin clot, and calculated the number of microvesicles of various origins.

Results. Women with hypertensive disease (HD) have increased levels of adhesion molecule JAM-A, factor IIa, soluble fibrinmonomer complexes, D-dimer, initial and stationary rates of fibrin clot formation and its size, as well as increased number of platelet, monocyte and endothelial microvesicles that are carrying and not carrying tissue factor. Numerous positive and negative correlations (from weak to moderate strength) between JAM-A content and some hemostatic parameters were revealed.

Conclusion. In patients with HD the readiness for thrombus formation is significantly increased. At hypertension JAM-A concentration not only increases, but its content significantly impacts coagulation processes in patients with HD.

References

  1. Kuznik B. I. Cellular and molecular mechanisms of the hemo stasis system in norm and pathology [Kletochnye i moleku lyarnye mekhanizmy sistemy gemostaza v norme i patologii]. Chita: Ekspress-izdatel’stvo. 2010: 832 s (in Russ.).
  2. Kuznik B. I., Vitkovsky Y. A., Gvozdeva O. V. et al. Lympho cyte-Platelet Crosstalk in Graves’ Disease. Am J Med Sci. 2014; 347 (3): 206–10.
  3. Romanyuk S. V., Vitkovsky Yu. A. Lymphocytic-platelet adhesion and platelet aggregation in patients with stable angina and acute coronary syndrome [Limfocitarno-trombocitarnaya adgeziya i agregaciya trombocitov u bol’nyh so stabil’noj stenokardiej i ostrym koronarnym sindromom]. Zabajkal’skij medicinskij vest nik. 2014; 4: 59–65 (in Russ.).
  4. Shenkman B., Brill I., Solpov A. et al. CD4+ lymphocytes require platelet for adhesion to immobilized fibronectin in flow: Role of β1 (CD29)-, β2 (CD18)-related integrins and non integrin receptors. Cell Immunol. 2006; 242 (1): 52–9.
  5. Sladojevic N., Stamatovic S. M., Keep R. F. et al. Inhibition of junctional adhesion molecule-A/LFA interaction attenuates leukocyte trafficking and inflammation in brain ischemia/ reperfusion injury. Neurobiol Dis. 2014; 67: 57–70.
  6. Stepanov A. V., Kradenov A. V. Leukocyte fibrinolysis in thrombolytic therapy [Lejkocitarnyj fibrinoliz v tromboliticheskoj terapii]. Zabajkal’skij medicinskij vestnik. 2015; 1: 125–8 (in Russ.).
  7. Naik M. U., Caplan J. L., Naik U. P. Junctional adhesion molecule-A suppresses platelet integrin αIIbβ3 signaling by recruiting Csk to the integrin-c-Src complex. Blood. 2014; 123 (9): 1393–402.
  8. Kuznik B. I., Khavinson V. Kh., Tarnovskaya S. I. et al. Adhesive molecule JAM-A and molecular mechanisms of agerelated pathology: a review of the literature and its own data [Adgezivnaya molekula JAM-A i molekulyarnye mekhanizmy vozrastnoj patologii: obzor literatury i sobstvennyh dannyh]. Uspekhi gerontologii. 2015; 28 (4): 656–68 (in Russ.).
  9. Ong K. L., Leung R. Y., Babinska A. et al. Elevated plasma level of soluble F11 receptor/junctional adhesion molecule-A (F11R/ JAM-A) in hypertension. Am J Hypertens. 2009; 22 (5): 500–5.
  10. Xu H., Oliveira-Sales E. B., McBride F. et al. Upregulation of junctional adhesion molecule-A is a putative prognostic marker of hypertension. Cardiovasc Res. 2012; 96 (3): 552–60 (doi: 10.1093/cvr/cvs273).
  11. Barkagan Z. S., Momot A. P. Diagnosis and controlled therapy of hemostasis disorders [Diagnostika i kontroliruemaya terapiya narushenij gemostaza]. Moskva: N’yudiamed-AO. 2008: 292 s (in Russ.).
  12. Panteleev M. A., Vasiliev S. A., Sinauridze E. I. et al. Practical coagulation [Prakticheskaya koagulologiya]. Moskva: Prakticheskaya medicina. 2011: 190 s (in Russ.).
  13. Kuznik B. I., Bogdanov I. G., Isakova N. V. et al. Thrombodynamic properties of arterial and venous blood in patients with ischemic heart disease in the preoperative and early postoperative periods with coronary shunting [Trombodinamicheskie svojstva arterial’noj i venoznoj krovi u bol’nyh IBS v dooperacionnom i rannem posleoperacionnom periodah pri vypolnenii koronarnogo shuntirovaniya]. Patologicheskaya fiziologiya i ehksperimental’naya terapiya. 2015; 1: 39–45 (in Russ.).
  14. Panchenko E. P., Dobrovolsky A. B. Thrombosis in cardiology. Mechanisms of development and the possibility of therapy [Mekhanizmy razvitiya i vozmozhnosti terapii]. Moskva: Sport i kul’tura. 1999: 463 s (in Russ.).
  15. Boiko N. V., Shatokhin Y. V. Pathogenesis of nasal bleeding in the patients presenting with arterial hypertension. Vestn Otorinolaringol. 2015; 80 (5): 41–5.
  16. Bokarev I. N., Popova L. V., Kozlova Т. V. Thrombosis and antithrombotic therapy in clinical practice [Trombozy i protivotromboticheskaya terapiya v klinicheskoj praktike]. Moskva: MIA. 2009: 510 s (in Russ.).
  17. Sesso H. D., Jiménez M. C., Wang L. et al. Plasma Inflammatory Markers and the Risk of Developing Hypertension in Men. J Am Heart Assoc. 2015; 4 (9): e001 802 (doi: 10.1161/ JAHA.115.001 802).
  18. Preston R. A., Jy W., Jimenez J. J. et al. Effects of severe hypertension on endothelial and platelet microparticles. Hypertension. 2003; 41 (2): 211–7.
  19. Zubairov M. D., Zubairova L. D. Microvesicles in the blood: functions and their role in thrombogenesis: monograph [Mikrovezikuly v krovi: funkcii i ih rol’ v tromboobrazovanii: monografiya]. Moskva: GEOTAR-Media. 2009: 167 s (in Russ.).
  20. Zubairov M. D. Molecular basis of blood clotting and thrombogenesis [Molekulyarnye osnovy svyortyvaniya krovi i tromboobrazovaniya]. Kazan’: FEN. 2000: 367 s (in Russ.).
  21. Lipets E., Vlasova O., Urnova E. et al. Circulating ContactPathway-Activating Microparticles Together with Factors IXa and XIa Induce Spontaneous Clotting in Plasma of Hematology and Cardiologic Patients. PLoS ONE. 2014; 9 (1): 1–11.
  22. Aatonen M., Grönholm М., Siljander Р. R. Platelet-derived microvesicles: multitalented participants in intercellular communication. Semin Thromb Hemost. 2012; 38: 102–13.
  23. Nielsen M. H., Irvine H., Vedel S. et al. The Impact of Lipoprotein-Associated Oxidative Stress on Cell-Specific Microvesicle Release in Patients with Familial Hypercholesterolemia. Oxid Med Cell Longev. 2016; 2016: Article ID 2 492 858 (doi: 10.1155/2016/2 492 858).
  24. Alexandru N., Badila E., Weiss E. et al. Microparticles: From Biogenesis to Biomarkers and Diagnostic Tools in Cardiovascular Disease. Curr Stem Cell Res Ther. 2015 [Epub ahead of print]. PMID: 26 647 911.
  25. Berezin A., Zulli A., Kerrigan S. et al. Predictive role of circulating endothelial-derived microparticles in cardiovascular diseases. Clin Biochem. 2015; 48 (9): 562–8.
  26. Sobocka M. B., Sobocki T., Babinska A. et al. Signaling pathways of the F11 receptor (F11R; a.k.a. JAM-1, JAM-A) in human platelets: F11R dimerization, phosphorylation and complex formation with the integrin GPIIIa. J Recept Signal Transduct Res. 2004; 134: 1557–72.
  27. Babinska A., Clement C. C., Swiatkowska M. et al. Development of new antiatherosclerotic and antithrombotic drugs utilizing F11 receptor (F11R/JAM-A) peptides. Biopolymers. 2014; 102 (4): 322–34.
  28. Naik M. U., Stalker T. J., Brass L. F., Naik U. P. JAM-A protects from thrombosis by suppressing integrin αIIbβ3-dependent outside-in signaling in platelets. Blood. 2012; 119 (14):3352–60.
  29. Vetrano S., Ploplis V. A., Sala E. et al. Unexpected role of anticoagulant protein C in controlling epithelial barrier integrity and intestinal inflammation. Proc Natl Acad Sci USA. 2011; 108 (49): 19 830–5.
  30. Cavusoglu E., Kornecki E., Sobocka M. B. et al. Association of plasma levels of F11 receptor/junctional adhesion moleculeA (F11R/JAM-A) with human atherosclerosis. J Am Coll Cardiol. 2007; 50 (18): 1768–76.
  31. Schmitt M. M., Fraemohs L., Hackeng T. M. et al. Atherogenic mononuclear cell recruitment is facilitated by oxidized lipoprotein-induced endothelial junctional adhesion molecule-A redistribution. Atherosclerosis. 2014; 234 (2): 254–64.
  32. Schmitt M. M., Megens R. T., Zernecke A. et al. Endothelial junctional adhesion molecule-a guides monocytes into flowdependent predilection sites of atherosclerosis. Circulation. 2014; 129 (1): 66–76.