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Updated: May 14, 2026
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Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Stimulation of platelet death by vancomycin
Syeda T Towhid1, Eva-Maria Schmidt, Alexander Tolios
1Department of Physiology, University of Tübingen, Germany.
Summary
Vancomycin antibiotic can cause platelet activation and apoptosis, a form of cell death. This process involves increased calcium, caspase-3 activation, and cell shrinkage, requiring calcium but not caspases.
Area of Science:
- Hematology
- Immunology
- Pharmacology
Background:
- Vancomycin, an antibiotic, is known to cause thrombocytopenia, a decrease in platelet count.
- This thrombocytopenia is thought to be immune-mediated, potentially involving platelet apoptosis.
- The effect of vancomycin on platelet apoptosis has not been previously investigated.
Purpose of the Study:
- To investigate the effect of vancomycin on platelet activation and apoptosis.
- To elucidate the mechanisms underlying vancomycin-induced platelet apoptosis.
Main Methods:
- Human platelets were exposed to vancomycin.
- Assays used included forward scatter (cell volume), annexin V-binding (phosphatidylserine exposure), Fluo-3 AM fluorescence (cytosolic Ca(2+) activity), ceramide quantification, and active caspase-3 immunofluorescence.
- Effects were assessed with and without extracellular calcium and in the presence of a caspase inhibitor.
Main Results:
- Vancomycin (≥1 µg/ml) decreased platelet volume, induced phosphatidylserine exposure, increased cytosolic Ca(2+) activity, activated caspase-3, and stimulated ceramide formation.
- Vancomycin also triggered thromboxane B2 release and upregulated surface expression of CD62P and activated integrin αllbβ3.
- These effects, particularly annexin V-binding and CD62P/integrin αllbβ3 upregulation, were blunted by calcium removal but not by a caspase inhibitor.
Conclusions:
- Vancomycin induces platelet activation and apoptosis.
- The process involves increased cytosolic Ca(2+), caspase-3 activation, cell membrane scrambling, and cell shrinkage.
- Platelet activation and membrane scrambling necessitate extracellular calcium, but caspase activation is not required.
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