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. Author manuscript; available in PMC: 2017 Jun 1.
Published in final edited form as: Circ Cardiovasc Genet. 2016 Apr 20;9(3):213–222. doi: 10.1161/CIRCGENETICS.115.001294

Figure 2.

Figure 2

Pharmaceutical inhibition of CDK4/6 reverses the PLT over-production phenotype of Cdkn2a-deficient strains. Chow-fed mice were bled at baseline and following 7, 16 or 21 days of 50 mg/kg PD0332991 treatment in chow diet. BM was collected at 21 days of treatment. A: PLT counts and mean platelet volume (MPV) from EDTA whole blood. N = 8 mice/group. B: Stem cell progenitor subpopulations from BM measured by flow cytometry. GMP (Lin−Sca1−c-kit+CD34intFcγRII/IIIhi), CMP (Lin−Sca1−c-kit+CD34intFcγRII/IIIint), MEP (Lin−Sca1−c-kit+CD34intFcγRII/IIIloCD71−CD41+), MkP (Lin−Sca1−c-kit+CD34intFcγRII/IIIloCD71−CD41+), and ErP (Lin−Sca1−c-kit+CD34intFcγRII/IIIloCD71+CD41−). N = 7-8 mice per group. C: MkP-CFUs derived from BM cells following 12 days of culture with 50 ng/ml TPO/10 ng/ml IL-3 and stained for acetylcholinesterase activity. D: Thrombin/anti-thrombin (T-AT) complex measured in sodium citrate plasma by commercially-available ELISA. Repeated measures (A) or one-way (B) ANOVA; Kruskal-Wallis non-parametric (C-D). NS, not significant.