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. 2010 May 5;38(16):5472–5478. doi: 10.1093/nar/gkq337

Figure 2.

Figure 2.

miR-155 expression is highest in BM stem cell pools, miR-155 is downstream of Hoxa9, and miR-155 down-regulates Pu.1. (A) miR-155 was expressed predominantly within the stem cell-enriched pools in FACS-fractionated BM progenitors. LT, long-term HSC pool; ST, short-term HSC pool; MPP, multipotential progenitor pool; CMP, common myeloid progenitor pool; MEP, myeloid–erythroid progenitor pool; and GMP, granulocyte–monocyte progenitor pool. (B) HOXA9-mediated expansion of clonogenic myeloid progenitors is blunted in miR-155-deficient BM cells. 5-FU treated wild-type or miR-155−/−(C) BM cells were infected with HOXA9-GFP or GFP control retroviral vectors and then plated for myeloid colony forming capacity as described in ‘Materials and methods’ section (n = 4). There was a significant difference (P < 0.018) between HOXA9 induction of myeloid colonies in wild-type BM cells versus miR-155−/−cells. (C) qPCR analysis showing that retroviral-mediated expression of miR-155 in Hoxa9−/−BM cells produced an ∼8-fold increase in miR-155 RNA. (D and E) Retroviral-mediated miR-155 expression in either wild-type or Hoxa9-deficient cells, respectively, resulted in an ∼2-fold decrease in Pu.1 protein, by western analysis.