Thromb Haemost 2018; 118(11): 1969-1981
DOI: 10.1055/s-0038-1673342
Atherosclerosis and Ischaemic Disease
Georg Thieme Verlag KG Stuttgart · New York

Monocytes of Different Subsets in Complexes with Platelets in Patients with Myocardial Infarction

Marina Loguinova*
1  Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia
,
Natalia Pinegina*
1  Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia
,
Valeria Kogan
2  Ariel University, Institute for Translational Research, Ariel, Israel
,
Murad Vagida
1  Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia
,
Anush Arakelyan
3  Section on Intercellular Interactions, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States
,
Alexander Shpektor
1  Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia
,
Leonid Margolis
3  Section on Intercellular Interactions, Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, Maryland, United States
,
Elena Vasilieva
1  Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia
› Author Affiliations
Funding This work was performed at the MSUMD. The work of M.L. and N.P. was supported by the Russian Science Foundation grant #18-75-10123. The work of E.V., M.V., L.M., and A.A. was supported, respectively, by the Intramural Programs of the MSUMD and NICHD.
Further Information

Publication History

29 December 2017

22 August 2018

Publication Date:
09 October 2018 (eFirst)

Abstract

Acute myocardial infarction (AMI) is associated with activation of various cells, including platelets that form monocyte–platelet complexes (MPCs). Here, we analysed MPC in vivo and in vitro and investigated the abilities of different monocyte subclasses to form MPC, the characteristics of the cells involved in MPC formation and MPC changes in AMI. We identified MPC by co-staining for platelet antigen CD41a and monocyte antigens CD14 and CD16. Platelet activation was evaluated from expression of phosphatidylserine as revealed by annexin V. Our results confirm published data and provide new information regarding the patterns of MPC in AMI patients. We found that the patterns of platelet aggregation with monocytes were different in AMI patients and controls: (1) in AMI patients, MPC formed by intermediate monocytes carry more platelets whereas in healthy controls more platelets aggregated with classical monocytes; (2) the numbers of MPC in AMI patients, being already higher than in controls, were further increased if these patients suffered various in-hospital complications; (3) on the basis of the CD41a fluorescence of the antibody-stained MPC, some of the aggregates seem to consist of monocytes and platelet-derived extracellular vesicles (EVs); (4) aggregation of monocytes with platelet EV occurred in in vitro experiments; and (5) these experiments demonstrated that monocytes from AMI patients aggregate with both platelets and platelet EVs more efficiently than do monocytes from controls. MPC in AMI patients may play an important role in this pathology.

Authors' Contributions

M.L.: Designed and performed the experiments, analysed the data and contributed to the writing of all sections of the manuscript. N.P.: Designed and performed the experiments, performed sample collection, collected patient information, analysed the data and contributed to the writing of the manuscript. V.K.: Analysed data and performed statistical analysis. M.V.: Analysed the data. A.A.: Analysed the data and contributed to the manuscript writing. A.S.: Conceived and designed the experiments and supervised the data analysis. L.M.: Conceived and designed the experiments, analysed the data and contributed to the writing of all sections of the manuscript. E. V.: Conceived and designed the experiments, supervised the work and contributed to the writing of the manuscript.


All authors approved the final manuscript.


* Marina Loguinova and Natalia Pinegina contributed equally to this work.


Supplementary Material