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Updated: Jun 13, 2026
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Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
Published on: November 29, 2024
Platelet senescence and phosphatidylserine exposure
Swapan Kumar Dasgupta1, Eduardo Rios Argaiz, Jose Emmanel Chedid Mercado
1Michael E. DeBakey Veterans Affairs Medical Center, Department of Pathology, Baylor College of Medicine.
Transfusion
|May 12, 2010
Summary
Phosphatidylserine exposure in stored platelets is mediated by cytochrome c release and caspase-3/ROCK1 activation, differing from activation-induced exposure. This finding is crucial for understanding platelet storage lesion and transfusion safety.
Area of Science:
- Hematology
- Cell Biology
- Biochemistry
Background:
- Phosphatidylserine exposure occurs during platelet activation, storage, and apoptosis.
- Mitochondrial cytochrome c release and loss of mitochondrial membrane potential (ΔΨm) are implicated in apoptosis-associated phosphatidylserine exposure.
Purpose of the Study:
- To investigate the role of cytochrome c release, ΔΨm, and cyclophilin D (CypD) in phosphatidylserine exposure during platelet activation and storage.
Main Methods:
- Flow cytometry was used to measure phosphatidylserine exposure and ΔΨm.
- Cyclosporin A and CypD-deficient platelets assessed CypD's role.
- Caspase-3 and Rho-associated kinase I (ROCK1) activation were analyzed via immunoblotting.
Main Results:
- Platelet activation-induced phosphatidylserine exposure correlated with ΔΨm loss, inhibited by cyclosporin A and absent in CypD-deficient platelets.
- Activation did not trigger cytochrome c release or caspase-3/ROCK1 activation.
- Stored platelets (>5 days) showed phosphatidylserine exposure linked to cytochrome c release and caspase-3/ROCK1 activation.
- ABT737 induced phosphatidylserine exposure via cytochrome c release independent of CypD.
Conclusions:
- Cytochrome c release and subsequent caspase-3/ROCK1 activation mediate phosphatidylserine exposure in stored platelets.
- This mechanism is distinct from activation-induced phosphatidylserine exposure.
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