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. Author manuscript; available in PMC: 2012 Jul 31.
Published in final edited form as: Br J Haematol. 2011 Jan 12;152(4):469–484. doi: 10.1111/j.1365-2141.2010.08548.x

Fig 1.

Fig 1

AHR null mice exhibit platelet defects and decreased steady-state Mk polyploidization. Peripheral blood from wild type (WT), AHR+/− (Het) and AHR-null (KO) mice was collected and examined for (A) platelet counts and (B) percentage of reticulated platelets. WT (black triangles), AHR+/− (open squares) and AHR-null mice (open circles) were subjected to bleeding time assays (n = 8 for WT and AHR+/−; n = 7 for AHR-null); shown is (C) the duration of the primary bleed and (D) average volume of blood lost during these experiments. A horizontal line indicates the average bleeding time for each genotype. (E) Bone marrow mononuclear cells were isolated and DNA content of CD41+ cells from WT, AHR+/− and AHR-null mice was examined by flow cytometry. Error bars for all experiments in this figure represent the SEM (n = 8). Asterisks denote statistically significant differences compared to WT mice; a single asterisk (*) represents P < 0·05 and two asterisks (**) represent P < 0·01.