Hamostaseologie 2023; 43(05): 338-347
DOI: 10.1055/a-2113-1134
Kim Jürgen Krott
1
Department of Vascular- and Endovascular Surgery, University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany
,
Tobias Feige
1
Department of Vascular- and Endovascular Surgery, University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany
,
Margitta Elvers
1
Department of Vascular- and Endovascular Surgery, University Hospital Düsseldorf, Heinrich-Heine-University, Düsseldorf, Germany
› Author Affiliations
Funding The study was supported by the Deutsche Forschungsgemeinschaft (DFG), grant number EL651/6-1; EL651/8-1 and Collaborative Research Centre TRR259 (Aortic Disease—grant no. 397484323) to M.E.
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Abstract
Platelets are main drivers of thrombus formation. Besides platelet aggregate formation, platelets interact with different blood cells such as red blood and white blood cells (RBCs, WBCs) and endothelial cells (ECs), to promote thrombus formation and inflammation. In the past, the role of different proteins in platelet adhesion, activation, and aggregate formation has been analyzed using platelets/mice with a genetic loss of a certain protein. These knock-out mouse models have been investigated for changes in experimental arterial thrombosis or hemostasis. In this review, we focused on the Maastricht flow chamber, which is a very elegant tool to analyze thrombus formation under flow using whole blood or different blood cell components of genetically modified mice. Besides, the interaction of platelets with RBCs, WBCs, and ECs under flow conditions has been evaluated with regard to thrombus formation and platelet-mediated inflammation. Importantly, alterations in thrombus formation as emerged in the flow chamber frequently reflect arterial thrombosis in different mouse models. Thus, the results of flow chamber experiments in vitro are excellent indicators for differences in arterial thrombosis in vivo. Taken together, the Maastricht flow chamber can be used to (1) determine the severity of platelet alterations in different knock-out mice; (2) analyze differences in platelet adhesion, aggregation, and activation; (3) investigate collagen and non–collagen-dependent alterations of thrombus formation; and (4) highlight differences in the interaction of platelets with different blood/ECs. Thus, this experimental approach is a useful tool to increase our understanding of signaling mechanisms that drive arterial thrombosis and hemostasis.
Keywords
arterial thrombus formation -
collagen -
glycoprotein VI -
platelets -
flow chamber
Publication History
Received: 02 May 2023
Accepted: 16 June 2023
Article published online:
19 October 2023
© 2023. Thieme. All rights reserved.
Georg Thieme Verlag KG
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