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van Geffen, Johanna P; Brouns, Sanne L N; Batista, Joana; McKinney, Harriet; Kempster, Carly; Nagy, Magdolna; Sivapalaratnam, Suthesh; Baaten, Constance C F M J; Bourry, Nikki; Frontini, Mattia; Jurk, Kerstin; Krause, Manuela; Pillitteri, Daniele; Swieringa, Frauke; Verdoold, Remco; Cavill, Rachel; Kuijpers, Marijke J E; Ouwehand, Willem H; Downes, Kate; Heemskerk, Johan W M
Haematologica (Roma), 06/2019, Letnik: 104, Številka: 6Journal Article
In combination with microspotting, whole-blood microfluidics can provide high-throughput information on multiple platelet functions in thrombus formation. Based on assessment of the inter- and intra-subject variability in parameters of microspot-based thrombus formation, we aimed to determine the platelet factors contributing to this variation. Blood samples from 94 genotyped healthy subjects were analyzed for conventional platelet phenotyping: i.e. hematologic parameters, platelet glycoprotein (GP) expression levels and activation markers (24 parameters). Furthermore, platelets were activated by ADP, CRP-XL or TRAP. Parallel samples were investigated for whole-blood thrombus formation (6 microspots, providing 48 parameters of adhesion, aggregation and activation). Microspots triggered platelet activation through GP Ib-V-IX, GPVI, CLEC-2 and integrins. For most thrombus parameters, inter-subject variation was 2-4 times higher than the intra-subject variation. Principal component analyses indicated coherence between the majority of parameters for the GPVI-dependent microspots, partly linked to hematologic parameters, and glycoprotein expression levels. Prediction models identified parameters per microspot that were linked to variation in agonist-induced α β activation and secretion. Common sequence variation of and , associated with GPVI-induced α β activation and secretion, affected parameters of GPVI-and CLEC-2-dependent thrombus formation. Subsequent analysis of blood samples from patients with Glanzmann thrombasthenia or storage pool disease revealed thrombus signatures of aggregation-dependent parameters that were subject-dependent, but not linked to GPVI activity. Taken together, this high-throughput elucidation of thrombus formation revealed patterns of inter-subject differences in platelet function, which were partly related to GPVI-induced activation and common genetic variance linked to GPVI, but also included a distinct platelet aggregation component.
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JCR | SNIP | JCR | SNIP | JCR | SNIP | JCR | SNIP |
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