Figure 5.
Hepcidin deletion worsens PV erythroid disease severity. (A) Liver Hamp1 mRNA expression relative to Hprt. (B) Serum hepcidin. (C-E) HGB (C), MCH (D), and HCT (E). (F) Terminal erythropoiesis in the BM determined by flow cytometry. Based on CD44 expression and FSC-A, Ter119+ cells were gated into 5 distinct populations: I , proerythroblasts; II, basophilic erythroblasts; III, polychromatic erythroblasts; IV, orthochromatic erythroblasts and reticulocytes; and V, RBCs. (G) MCV. (H) Liver and (I) spleen nonheme liver iron. (J) RBCs. Control, n = 6; iHamp-KO, n = 4; PV, n = 4; and PV × iHamp-KO, n = 7, except for panel B in which control, n = 3; PV, n = 3; and PV × iHamp-KO, n = 4. Kruskal-Wallis test for panels A,D,G, ordinary one-way ANOVA for panels B-C,E,H-J, or two-way ANOVA with Dunnett correction for multiple comparisons for panel F. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

Hepcidin deletion worsens PV erythroid disease severity. (A) Liver Hamp1 mRNA expression relative to Hprt. (B) Serum hepcidin. (C-E) HGB (C), MCH (D), and HCT (E). (F) Terminal erythropoiesis in the BM determined by flow cytometry. Based on CD44 expression and FSC-A, Ter119+ cells were gated into 5 distinct populations: I , proerythroblasts; II, basophilic erythroblasts; III, polychromatic erythroblasts; IV, orthochromatic erythroblasts and reticulocytes; and V, RBCs. (G) MCV. (H) Liver and (I) spleen nonheme liver iron. (J) RBCs. Control, n = 6; iHamp-KO, n = 4; PV, n = 4; and PV × iHamp-KO, n = 7, except for panel B in which control, n = 3; PV, n = 3; and PV × iHamp-KO, n = 4. Kruskal-Wallis test for panels A,D,G, ordinary one-way ANOVA for panels B-C,E,H-J, or two-way ANOVA with Dunnett correction for multiple comparisons for panel F. ∗P < .05; ∗∗P < .01; ∗∗∗P < .001; ∗∗∗∗P < .0001.

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