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Updated: Feb 4, 2026

Myocardial Infarction and Functional Outcome Assessment in Pigs
Published on: April 25, 2014
Monocytes of Different Subsets in Complexes with Platelets in Patients with Myocardial Infarction
Marina Loguinova1, Natalia Pinegina1, Valeria Kogan2
1Laboratory of Atherothrombosis, Moscow State University of Medicine and Dentistry, Moscow, Russia.
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.
Insights
Monocyte-platelet complexes (MPCs) are elevated in acute myocardial infarction (AMI) patients. In AMI, intermediate monocytes form more platelet-rich MPCs, and monocytes from AMI patients aggregate more efficiently with platelets and their extracellular vesicles.
Area of Science:
- Cardiovascular Biology
- Immunology
- Hematology
Background:
- Acute myocardial infarction (AMI) involves cellular activation, including platelet aggregation with monocytes to form monocyte-platelet complexes (MPCs).
- Understanding MPC formation and characteristics is crucial for elucidating AMI pathophysiology.
Purpose of the Study:
- To analyze in vivo and in vitro monocyte-platelet complexes (MPCs) in acute myocardial infarction (AMI) patients.
- To investigate monocyte subclass abilities in MPC formation, cellular characteristics, and changes in AMI.
Main Methods:
- MPCs identified by co-staining for CD41a (platelet) and CD14/CD16 (monocyte) antigens.
- Platelet activation assessed via phosphatidylserine expression using annexin V.
- In vitro experiments assessed monocyte aggregation with platelets and platelet-derived extracellular vesicles (EVs).
Main Results:
- In AMI patients, intermediate monocytes formed more platelet-rich MPCs compared to classical monocytes in controls.
- MPC numbers were higher in AMI patients and increased with in-hospital complications.
- Monocytes from AMI patients showed more efficient aggregation with both platelets and platelet EVs in vitro.
- Evidence suggests some MPCs may involve platelet-derived extracellular vesicles (EVs).
Conclusions:
- Monocyte-platelet complex patterns differ significantly between AMI patients and healthy controls.
- Increased MPC formation, particularly by intermediate monocytes and involving platelet EVs, may contribute to AMI pathology.
- These findings highlight MPCs as a potential factor in acute myocardial infarction progression.
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