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

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.

Platelets in Healthy and Disease States: From Biomarkers Discovery to Drug Targets Identification by Proteomics

“…Integrins also facilitate platelets to bind to ECM molecules and other cells playing an important role in cell signaling. Since platelet surface markers have, in general, short detectability in human blood, platelet-monocyte aggregates have been detected in several studies as a more sensitive and accurate marker that describes platelet activation and a prothrombotic state in diseases, like advanced atherosclerosis, stable coronary artery disease, acute myocardial infarction, systemic inflammatory and autoimmune disorders, and neoplasms [ 40 , 41 , 42 ]. Similarly, circulating PMPs, that are the most abundant microparticles in the bloodstream (approximately 70–90% of circulating microparticles), are considered as potential biological markers for platelet activation [ 43 ].…”

Platelet Functions During Extracorporeal Membrane Oxygenation. Platelet–Leukocyte Aggregates Analyzed by Flow Cytometry as a Promising Tool to Monitor Platelet Activation

“…Among all leukocytes, monocytes show the highest affinity for platelet P-selectin, followed by neutrophils; lymphocytes have the lowest affinity [23]. It was shown that among monocytes, different subclasses are involved in PLA, in normal subjects and in patients with myocardial infarction as well [24]. The formation of PLAs involves the release of mediators and mutual activation of both cell types.…”

“…Upon activation, platelet extracellular vesicles, measuring from 100 to 1000 nm, are released and circulated, and it cannot be ruled out that they form complexes with leukocytes [24]. Since these complexes are CD41-positive, they can hardly be distinguished from PLAs with platelets.…”

The Role of ROCK in Platelet–Monocyte Collaborative Induction of Thromboinflammation during Acute Coronary Syndrome

“…22,23 MPA levels were previously found to be higher in ACS patients. 5,24,25 Utilizing this knowledge, coronary-artery aspirates of STEMI patients with a ruptured atheroma were immunostained for platelets and monocytes. The results showed that MPAs remained within the coronary thrombus (►Fig.…”