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Procoagulant Platelet Characterization by Measuring Phosphatidylserine Exposure and Microvesicle Release from Human Purified Platelets
Published on: November 29, 2024
Diabetes Type 2: Circulating Phosphatidylserine-Expressing Platelets Regulate Whole Blood Agonist-Evoked Platelet
Petter Järemo1, Magnus Oweling2, Maria Edvardsson2,3,4
1Jaremo Vardbolag ABNorrköpingSweden.
TH Open : Companion Journal to Thrombosis and Haemostasis
|August 13, 2026
Summary
In type 2 diabetes, unprovoked phosphatidylserine (PS)-exposing platelets in vitro are linked to altered platelet reactivity. This suggests a connection between baseline platelet activation and responses to agonists in diabetic patients.
Area of Science:
- Hematology
- Endocrinology
- Cellular Biology
Background:
- Platelet activation involves phosphatidylserine (PS) exposure, fibrinogen receptor (αIIbβ3) activation, and lysosomal exocytosis.
- Platelet activation pathways can be assessed by measuring surface annexin V, activated fibrinogen receptor (PAC-1), and lysosomal-associated membrane protein (LAMP-1).
- This study investigates the link between unprovoked PS exposure on circulating platelets and agonist-induced platelet responses in type 2 diabetes mellitus (T2DM).
Purpose of the Study:
- To determine if unprovoked phosphatidylserine (PS) exposure on circulating platelets in T2DM patients correlates with whole blood (WB) agonist-induced platelet responses.
- To analyze the relationship between density-separated platelet subpopulations and their reactivity to various agonists in vitro.
Main Methods:
- Thirty-five T2DM patients provided informed consent.
- Platelets were separated into density subpopulations using a Percoll gradient.
- Flow cytometry analyzed surface annexin V (mean fluorescence intensity [MFI]) on platelet subfractions ex vivo and whole blood (WB) agonist-induced responses (annexin V, PAC-1, LAMP-1) to α-thrombin, CRP-XL, and ADP in vitro.
Main Results:
- A close association was observed between surface annexin V (MFI) in most platelet subfractions and WB agonist-induced annexin V (MFI) in normal-sized platelets.
- PS-expressing platelets were inversely correlated with WB agonist-evoked PAC-1 (MFI) for all agonists used.
- PS-expressing platelets showed an inverse correlation with LAMP-1 (MFI) for CRP-XL and ADP-induced activation.
Conclusions:
- Unprovoked surface PS exposure on density-separated platelets in T2DM is closely linked to platelet reactivity.
- The findings suggest that baseline PS exposure may modulate agonist-induced platelet activation pathways, including fibrinogen receptor activation and lysosomal exocytosis, in T2DM.
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