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. 2016 Oct 6;1(16):e88643. doi: 10.1172/jci.insight.88643

Figure 9. In vivo administration of LIM kinase inhibitor (LIMKi) increases the platelet count and reduces the mean platelet volume in type 2B mutant vWF/p.V1316M (2B) mice but does not reverse the hemostatic defect.

Figure 9

Whole-blood platelet counts in WT (A) and 2B mice (B) of DMSO-treated and LIMKi-treated mice before and after 3 injections of LIMKi (30 mg/kg) or DMSO (1.6 μl/g body weight) at various times. n = 3. Mean platelet volume (MPV) (C) of DMSO-treated 2B mice and LIMKi-treated 2B mice. n = 4–12 mice in each group. Statistical significance was determined by 1-way ANOVA followed by Dunnett’s test. *P < 0.05, **P < 0.01, ***P < 0.001. NS, not significant. (D) Tail bleeding time in WT (n = 3) and 2B mice (n = 6 and 9) of DMSO-treated mice and LIMKi-treated mice after 3 injections of LIMKi (30 mg/kg) or DMSO. Integrin αIIbβ3 expression (n = 4) (E) and activation (n = 3) (F) were assessed by flow cytometry using a CD41 antibody and integrin αIIbβ3 mAb (JON/A) specific for the activated conformation of the mouse integrin, respectively. The level of activated integrin is indicated by the mean fluorescence intensity (MFI) ratio JON/A:CD41, calculated with the WT JON/A:CD41 ratio equal to 1.