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.

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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