Figure 1.
Figure 1. Binding of platelets to endothelial-released VWF. (A) Snapshot taken during a representative microfluidic experiment. HUVECs were perfused at a constant shear stress of 6 dyne/cm2. VWF release was induced by 50 µM of histamine, and adhering fluorescent platelets (false color-coded in white) were tracked by fluorescence microscopy. VWF fibers (green) were stained with a FITC-conjugated antibody during the experiment. Scale bar, 100 µm. (B) VWF-mediated binding of platelets (white) to the endothelium. The endothelial gylcocalyx was manipulated through treatment with heparinase-I (hep’nase), COS, or both compounds (COS + hep’nase). Only histamine-treated HUVECs were used as control (CTL). Scale bar, 100 µm. (C) Quantitative evaluation of the VWF-dependent platelet coverage (n = 3-9). *P ≤ .05, **P ≤ .01 (1-way analysis of variance and Bonferroni post hoc test). rel., relative.

Binding of platelets to endothelial-released VWF. (A) Snapshot taken during a representative microfluidic experiment. HUVECs were perfused at a constant shear stress of 6 dyne/cm2. VWF release was induced by 50 µM of histamine, and adhering fluorescent platelets (false color-coded in white) were tracked by fluorescence microscopy. VWF fibers (green) were stained with a FITC-conjugated antibody during the experiment. Scale bar, 100 µm. (B) VWF-mediated binding of platelets (white) to the endothelium. The endothelial gylcocalyx was manipulated through treatment with heparinase-I (hep’nase), COS, or both compounds (COS + hep’nase). Only histamine-treated HUVECs were used as control (CTL). Scale bar, 100 µm. (C) Quantitative evaluation of the VWF-dependent platelet coverage (n = 3-9). *P ≤ .05, **P ≤ .01 (1-way analysis of variance and Bonferroni post hoc test). rel., relative.

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