| Literature DB >> 30300910 |
Marina Loguinova1, Natalia Pinegina1, Valeria Kogan2, Murad Vagida1, Anush Arakelyan3, Alexander Shpektor1, Leonid Margolis3, Elena Vasilieva1.
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. Georg Thieme Verlag KG Stuttgart · New York.Entities:
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Year: 2018 PMID: 30300910 PMCID: PMC7000167 DOI: 10.1055/s-0038-1673342
Source DB: PubMed Journal: Thromb Haemost ISSN: 0340-6245 Impact factor: 5.249