Figure 6.
Drug correction of function and platelet-release defects with RepSox. (A) 3 × 106 shNT-, shRX-, or shRX+RepSox (shRX+RS)–megakaryocytes were infused into NSG mice. At each time point, mouse peripheral blood was withdrawn to monitor human platelet level. The peripheral blood samples were stained with hCD41 and mCD41 antibodies and analyzed by flow cytometry for human vs mouse platelets as in Figure 2. Mean ± 1 SD are shown. N = 3 per arm. ∗P < .05 and ∗∗P < .001 comparing shRX vs shRX+RS studies. (B) Study as in panel A. P-selectin levels on released human platelets in mouse blood were measured by flow cytometry under activation with various concentrations of TRAP. N = 3 per arm. ∗P ≤ .05 and ∗∗P ≤ .001 by 1-way ANOVA comparing shRX vs shRX+RS studies.

Drug correction of function and platelet-release defects with RepSox. (A) 3 × 106 shNT-, shRX-, or shRX+RepSox (shRX+RS)–megakaryocytes were infused into NSG mice. At each time point, mouse peripheral blood was withdrawn to monitor human platelet level. The peripheral blood samples were stained with hCD41 and mCD41 antibodies and analyzed by flow cytometry for human vs mouse platelets as in Figure 2. Mean ± 1 SD are shown. N = 3 per arm. ∗P < .05 and ∗∗P < .001 comparing shRX vs shRX+RS studies. (B) Study as in panel A. P-selectin levels on released human platelets in mouse blood were measured by flow cytometry under activation with various concentrations of TRAP. N = 3 per arm. ∗P ≤ .05 and ∗∗P ≤ .001 by 1-way ANOVA comparing shRX vs shRX+RS studies.

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