Microfluidic whole blood testing of platelet response to pharmacological agents
Li R, Grosser T, Diamond SL (2017)
Platelets 28(5): 457-462.
Zeitschriftenaufsatz
| Veröffentlicht | Englisch
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Autor*in
Li, Ruizhi;
Grosser, TiloUniBi
;
Diamond, Scott L.
![](https://pub.uni-bielefeld.de/images/icon_orcid.png)
Abstract / Bemerkung
Platelets present a number of intracellular and transmembrane targets subject to pharmacological modulation, either for cardiovascular disease reduction or as an unintended drug response. Microfluidic devices allow human blood to clot on a defined surface under controlled hemodynamic and pharmacological conditions. The potencies of a number of antiplatelet and anticancer drugs have been tested with respect to platelet deposition on collagen under flow. Inhibitors of cyclooxygenase-1 (COX-1) reduce platelet deposition, either when added ex vivo to blood or ingested orally by patients prior to testing. Some individuals display a functional “aspirin-insensitivity” in microfluidic assay. When certain nonsteroidal anti-inflammatory drugs (NSAIDs) are taken orally, they block COX-1 acetylation by aspirin with concomitant reduction of aspirin efficacy against platelets in microfluidic assay. Both P2Y1 and P2Y12 inhibitors reduce platelet deposition under flow, as do NO donors and iloprost that target the guanylate cyclase and the prostacyclin receptor, respectively. In a microfluidic assay of 37 kinase inhibitors, dasatinib had potent antiplatelet activity, while bosutinib was less potent. Dasatinib and bosutinib have known profiles against numerous kinases, revealing overlapping and nonoverlapping activities relevant to their unique actions against platelets. Also, dasatinib caused a marked and specific inhibition of GPVI signaling induced by convulxin, consistent with a dasatinib-associated bleeding risk. Microfluidic devices facilitate drug library screening, dose–response testing, and drug–drug interaction studies. Kinase inhibitors developed as anticancer agents may present antiplatelet activities that are detectable by microfluidic assay and potentially linked to bleeding risks.
Erscheinungsjahr
2017
Zeitschriftentitel
Platelets
Band
28
Ausgabe
5
Seite(n)
457-462
ISSN
0953-7104
eISSN
1369-1635
Page URI
https://pub.uni-bielefeld.de/record/2965314
Zitieren
Li R, Grosser T, Diamond SL. Microfluidic whole blood testing of platelet response to pharmacological agents. Platelets. 2017;28(5):457-462.
Li, R., Grosser, T., & Diamond, S. L. (2017). Microfluidic whole blood testing of platelet response to pharmacological agents. Platelets, 28(5), 457-462. https://doi.org/10.1080/09537104.2016.1268254
Li, Ruizhi, Grosser, Tilo, and Diamond, Scott L. 2017. “Microfluidic whole blood testing of platelet response to pharmacological agents”. Platelets 28 (5): 457-462.
Li, R., Grosser, T., and Diamond, S. L. (2017). Microfluidic whole blood testing of platelet response to pharmacological agents. Platelets 28, 457-462.
Li, R., Grosser, T., & Diamond, S.L., 2017. Microfluidic whole blood testing of platelet response to pharmacological agents. Platelets, 28(5), p 457-462.
R. Li, T. Grosser, and S.L. Diamond, “Microfluidic whole blood testing of platelet response to pharmacological agents”, Platelets, vol. 28, 2017, pp. 457-462.
Li, R., Grosser, T., Diamond, S.L.: Microfluidic whole blood testing of platelet response to pharmacological agents. Platelets. 28, 457-462 (2017).
Li, Ruizhi, Grosser, Tilo, and Diamond, Scott L. “Microfluidic whole blood testing of platelet response to pharmacological agents”. Platelets 28.5 (2017): 457-462.
Daten bereitgestellt von European Bioinformatics Institute (EBI)
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Daten bereitgestellt von Europe PubMed Central.
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Daten bereitgestellt von Europe PubMed Central.
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