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. 2019 Jul 4;105(4):1095–1106. doi: 10.3324/haematol.2018.214460

Figure 1.

Figure 1.

Exposure of phosphatidylserine by Wiskott-Aldrich syndrome platelets upon fibrinogen binding. (A) Confocal microscopy images of healthy (left) and Wiskott-Aldrich syndrome (WAS) (right) platelets after spreading for 30 min on a fibrinogen surface in the presence of 1.5 μM Ca2+. The platelets are labeled with CD61 (green) and annexin V (red); scale bar: 10 μm. (B) Phosphatidylserine-positive (PS+) fraction of platelets from the WAS patients (27 patients, >7,500 cells), adult healthy (18 donors, >6,500 cells) and 0- to 7-year old children without WAS (6 children, age: 0, 0, 2, 3, 4, 7 years, 2,300 platelets) on a fibrinogen surface. (C) PS+ fraction of WAS platelets on the fibrinogen surface, showing a comparison of romiplostim-treated and untreated WAS patients, P=0.94. (D) Monafram-coated coverslips did not change the PS+ fraction, P=0.86, n=4, 2,500 platelets. w/o: without; FG: fibrinogen.