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. 2019 Feb 28;104(12):2493–2500. doi: 10.3324/haematol.2018.206250

Figure 2.

Figure 2.

Platelet desialylation by 2B von Willebrand disease (vWF) in vitro occurs on N-glycans. (A) A histogram of RCA lectin binding on wild-type (WT) mouse platelets in PRP treated with vWF-deficient plasma (vWF-dp), WT plasma or 2B plasma. The fold change in each experiment was calculated relative to the binding obtained with vWF-deficient plasma, set to 1. The mean±Standard Deviation (SD) values (n=3 experiments) were compared using a one-way ANOVA and Dunnett’s post-test; **P<0.01. (B) A histogram of RCA lectin binding to washed WT mouse platelets treated with WT or 2B mouse vWF (p.V1316M). (C) Histograms of RCA and ECL binding (for β-galactose exposure) on washed WT mouse platelets treated with 0.2 μg/mL WT or 2B mouse vWF. The fold change in each experiment was calculated relative to the baseline value (in the absence of vWF), set to 1. The mean±SD values (n=4 experiments) were compared using a one-way ANOVA and Dunnett’s post-test; **P<0.01). (D) Flow cytometric analysis of NEU1 expression on washed WT mouse platelets treated with 0.2 μg/mL WT or 2B mouse vWF; *P<0.05. (E) Histograms of MALII lectin binding (for α-2,3-linked sialic acids on O-glycans) on washed WT mouse platelets treated with 0.2 μg/mL WT or 2B mouse vWF. (F) Flow cytometric analysis of WT platelets after treatment (or not) with PNGase F and staining with RCA and MALII lectin. The data are representative of three independent experiments. (G) A histogram of RCA binding on washed WT mouse platelets treated with 0.2 μg/mL WT or 2B vWF. Platelets were then treated (or not) with PNGase F. The mean±SD values (n=3 experiments) were compared using a one-way ANOVA and Dunnett’s post-test. ***P<0.001.