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Updated: Apr 4, 2026

Comprehensive Analysis of Procoagulant Platelets Exhibiting Features of Necrosis, Apoptosis and Platelet Activation
Published on: May 23, 2025
Coordinated Membrane Ballooning and Procoagulant Spreading in Human Platelets.
Ejaife O Agbani1, Marion T J van den Bosch2, Ed Brown2
1From School of Physiology & Pharmacology, University of Bristol, United Kingdom (E.O.A., M.T.J.v.d.B., E.B., C.M.W., I.H., A.W.P.; Department of Biochemistry, Cardiovascular Research Institute Maastricht (CARIM), University of Maastricht, The Netherlands (N.J.A.M., J.M.E.M.C., J.W.M.H.); and Welsh Blood Service and Arthur Bloom Haemophilia Centre, School of Medicine, Cardiff University, United Kingdom (P.W.C.). a.poole@bristol.ac.uk e.agbani@bristol.ac.uk.
Platelet ballooning, a key part of hemostasis, is driven by fluid and ion entry, crucial for amplifying coagulation during thrombosis.
Area of Science:
- Hematology
- Cell Biology
- Biophysics
Background:
- Platelets are essential for hemostasis, forming structures at injury sites.
- Platelet transformation into balloonlike structures during hemostasis is not fully understood.
Purpose of the Study:
- To investigate the physiological relevance of platelet ballooning.
- To elucidate the cellular and molecular mechanisms of platelet membrane ballooning.
Main Methods:
- Utilized 4D live-cell imaging and electron microscopy.
- Studied human platelets adherent to collagen.
- Investigated the role of ion and water transport.
Main Results:
- Platelet ballooning, termed procoagulant spreading, involves phosphatidylserine exposure and fluid entry.
- Ballooning is irreversible, distinct from blebbing, and requires Na(+), Cl(-), and water influx.
- Inhibition of ion/water entry, or Ano-6 deficiency (Scott syndrome), reduced ballooning and thrombin generation.
- Acetazolamide blocked ballooning in vitro and suppressed thrombosis in vivo.
Conclusions:
- Platelet ballooning and procoagulant spreading are driven by fluid entry.
- These processes amplify localized coagulation, playing a critical role in thrombosis.
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