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Flow Cytometry Analysis of Tissue Factor Expression in Human Platelets
Published on: November 22, 2024
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Platelet subpopulation bearing leukocyte specific antigen and tissue factor
Z A Gabbasov1, O S Saburova1, O A Antonova1
1Russian Cardiology Research and production Complex, Russian Ministry of Health, Moscow, Russia.
Doklady. Biochemistry and Biophysics
|January 7, 2017
Summary
Platelets expressing CD45 and tissue factor (TF) were found in myocardial infarction (MI) patients. Their levels increased 8-12 days post-MI, suggesting a role in clotting after heart attack.
Area of Science:
- Cardiovascular Biology
- Hematology
- Immunology
Background:
- Platelets play a crucial role in hemostasis and thrombosis.
- Leukocyte antigen CD45 is typically found on leukocytes, not platelets.
- Tissue factor (TF) initiates the extrinsic pathway of blood coagulation.
Purpose of the Study:
- To investigate the presence and kinetics of CD45-positive platelets in patients with myocardial infarction (MI).
- To determine the co-expression of tissue factor (TF) on CD45-positive platelets in MI patients.
- To explore the potential origin of CD45-positive platelets in the context of MI.
Main Methods:
- Flow cytometry was used to identify and quantify platelets expressing CD45 and TF.
- Blood samples were collected from MI patients and healthy donors at different time points.
Main Results:
- Platelets expressing CD45 (CD45+) and co-expressing TF (CD45+/TF+) were detected in both MI patients and healthy donors.
- The number of CD45+ and CD45+/TF+ platelets was comparable between MI patients and controls on day 1 post-MI.
- A significant increase in CD45+ and CD45+/TF+ platelets was observed in MI patients 8-12 days after MI onset, reaching up to 5-6% and 2-3% respectively.
Conclusions:
- CD45-positive platelets, some expressing TF, are present in circulation and increase after myocardial infarction.
- The elevated levels of CD45+/TF+ platelets suggest a potential role in the thrombotic complications following MI.
- These CD45+/TF+ platelets may arise from interactions between platelets and leukocytes or leukocyte-derived microparticles.
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