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MIR233  is genetically or epigenetically silenced in a subset of acute myeloid leukemia (AML).  MIR223  is normally expressed throughout myeloid differentiation and highly expressed in hematopoietic stem cells (HSCs). However, the contribution of  MIR223  loss to leukemic transformation and HSC function is largely unknown. Herein, we characterize HSC function and myeloid differentiation in  Mir223  deficient mice. We show that  Mir223  loss results in a modest expansion of myeloid progenitors, but is not sufficient to induce a myeloproliferative disorder. Loss of  Mir223  had no discernible effect on HSC quiescence, long-term repopulating activity, or self-renewal capacity. These results suggest that  MIR223  loss is likely not an initiating event in AML but may cooperate with other AML associated oncogenes to induce leukemogenesis.

MicroRNA-223 Regulates Granulopoiesis but Is Not Required for HSC Maintenance in Mice