Figure 4.
Figure 4. Platelet function is not impaired by the absence of RUNX1C. (A) Morphologic analysis of peripheral blood cells, in particular platelets. May-Grünwald-Giemsa–stained peripheral blood films. The bottom panel consists of enlarged images of sections indicated in the top panel. Representative images from 4 independent experiments are shown. (B-D) Assessment of platelet aggregation in vitro. (B) Representative FACS plots of CD9 APC and CD9 PE staining of unstimulated PRP and PRP treated with various agonists as indicated. (C-D) Quantitation of platelet aggregation (percent CD9 APC PE double positive events) in unstimulated and stimulated PRP (C, P values shown as compared with unstimulated) and fold increase in CD9 APC PE double positive aggregates following treatment with various agonists with respect to unstimulated PRP (D) (N = 4). *P < .05, **P < .01, ***P < .001, ****P < .0001. APC, allophycocyanin; PMA, phorbol 12-myristate 13-acetate.

Platelet function is not impaired by the absence of RUNX1C. (A) Morphologic analysis of peripheral blood cells, in particular platelets. May-Grünwald-Giemsa–stained peripheral blood films. The bottom panel consists of enlarged images of sections indicated in the top panel. Representative images from 4 independent experiments are shown. (B-D) Assessment of platelet aggregation in vitro. (B) Representative FACS plots of CD9 APC and CD9 PE staining of unstimulated PRP and PRP treated with various agonists as indicated. (C-D) Quantitation of platelet aggregation (percent CD9 APC PE double positive events) in unstimulated and stimulated PRP (C, P values shown as compared with unstimulated) and fold increase in CD9 APC PE double positive aggregates following treatment with various agonists with respect to unstimulated PRP (D) (N = 4). *P < .05, **P < .01, ***P < .001, ****P < .0001. APC, allophycocyanin; PMA, phorbol 12-myristate 13-acetate.

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