MicroRNA-223 regulates granulopoiesis but is not required for HSC maintenance in mice

PloS One
Maria C TrissalDaniel C Link

Abstract

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.

References

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Citations

Oct 6, 2016·Oncotarget·Qiong LiaoGuosheng Jiang
Apr 4, 2017·Cell Biology International·Xiaman WangAili He
Aug 10, 2019·Proceedings of the National Academy of Sciences of the United States of America·Gayathri SrinivasanRobert Hromas
Dec 5, 2020·Science·Dionna M KasperStefania Nicoli
Aug 7, 2021·Biology·Mateusz NowickiAnna Szmigielska-Kapłon

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Methods Mentioned

BETA
flow cytometry
FACS

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