Type

Journal Article

Authors

Marek W Radomski
John F Gilmer
Despina Bazou
Carlos Medina
Krzysztof A Tomaszewski
Maria J Santos-Martinez
Carlos Medina Martin

Subjects

Pharmacology

Topics
platelet aggregation quartz crystal microbalance nitric oxide donors dissipation platelet nanoparticle adenosine diphosphate matrix metalloproteinase 2 platelet rich plasma platelet activation nanoscience materials thromboxane a2

Pharmacological characterization of nanoparticle-induced platelet microaggregation using quartz crystal microbalance with dissipation: comparison with light aggregometry. (2015)

Abstract Engineered nanoparticles (NPs) can induce platelet activation and aggregation, but the mechanisms underlying these interactions are not well understood. This could be due in part to use of devices that study platelet function under quasi-static conditions with low sensitivity to measure platelet microaggregation. Therefore, in this study we investigated the pharmacological pathways and regulators of NP-induced platelet microaggregation under flow conditions at nanoscale using quartz crystal microbalance with dissipation (QCM-D) and compared the data thus obtained with those generated by light aggregometry. Blood was collected from healthy volunteers, and platelet-rich plasma was obtained. Thrombin receptor-activating peptide, a potent stimulator of platelet function, and pharmacological inhibitors were used to modulate platelet microaggregation in the presence/absence of silica (10 nm and 50 nm) and polystyrene (23 nm) NPs. Light aggregometry was used to study platelet aggregation in macroscale. Optical, immunofluorescence, and scanning electron microscopy were also used to visualize platelet aggregates. Platelet microaggregation was enhanced by thrombin receptor-activating peptide, whereas prostacyclin, nitric oxide donors, acetylsalicylic acid, and phenanthroline, but not adenosine diphosphate (ADP) blockers, were able to inhibit platelet microaggregation. NPs caused platelet microaggregation, an effect not detectable by light aggregometry. NP-induced microaggregation was attenuated by platelet inhibitors. NP-induced platelet microaggregation appears to involve classical proaggregatory pathways (thromboxane A2-mediated and matrix metalloproteinase-2-mediated) and can be regulated by endogenous (prostacyclin) and pharmacological (acetylsalicylic acid, phenanthroline, and nitric oxide donors) inhibitors of platelet function. Quartz crystal microbalance with dissipation, but not light aggregometry, is an appropriate method for studying NP-induced microaggregation.
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Full list of authors on original publication

Marek W Radomski, John F Gilmer, Despina Bazou, Carlos Medina, Krzysztof A Tomaszewski, Maria J Santos-Martinez, Carlos Medina Martin

Experts in our system

1
Marek W Radomski
Trinity College Dublin
Total Publications: 44
 
2
John Gilmer
Trinity College Dublin
Total Publications: 28
 
3
Carlos Medina
Trinity College Dublin
Total Publications: 23
 
4
Maria Jose Santos-Martinez
Trinity College Dublin
Total Publications: 29
 
5
Carlos Medina Martin
Trinity College Dublin
Total Publications: 28