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A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset

Author

Listed:
  • Dorothée Selimoglu-Buet

    (Gustave Roussy Cancer Center)

  • Julie Rivière

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Hussein Ghamlouch

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Laura Bencheikh

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Catherine Lacout

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Margot Morabito

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • M’boyba Diop

    (Gustave Roussy Cancer Center)

  • Guillaume Meurice

    (Gustave Roussy Cancer Center)

  • Marie Breckler

    (Gustave Roussy Cancer Center)

  • Aurélie Chauveau

    (Gustave Roussy Cancer Center
    Centre Hospitalier Régional Universitaire)

  • Camille Debord

    (Gustave Roussy Cancer Center
    Centre Hospitalier Régional Universitaire)

  • Franck Debeurme

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Raphael Itzykson

    (Gustave Roussy Cancer Center
    Assistance Publique-Hôpitaux de Paris)

  • Nicolas Chapuis

    (Institut Cochin)

  • Christophe Willekens

    (Gustave Roussy Cancer Center
    Université Paris Diderot
    Gustave Roussy Cancer Center)

  • Orianne Wagner-Ballon

    (Hôpital Henri-Mondor)

  • Olivier A. Bernard

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine)

  • Nathalie Droin

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine
    Gustave Roussy Cancer Center)

  • Eric Solary

    (Gustave Roussy Cancer Center
    Université Paris-Sud, Faculté de Médecine
    Gustave Roussy Cancer Center)

Abstract

Non-classical monocyte subsets may derive from classical monocyte differentiation and the proportion of each subset is tightly controlled. Deregulation of this repartition is observed in diverse human diseases, including chronic myelomonocytic leukemia (CMML) in which non-classical monocyte numbers are significantly decreased relative to healthy controls. Here, we identify a down-regulation of hsa-miR-150 through methylation of a lineage-specific promoter in CMML monocytes. Mir150 knock-out mice demonstrate a cell-autonomous defect in non-classical monocytes. Our pulldown experiments point to Ten-Eleven-Translocation-3 (TET3) mRNA as a hsa-miR-150 target in classical human monocytes. We show that Tet3 knockout mice generate an increased number of non-classical monocytes. Our results identify the miR-150/TET3 axis as being involved in the generation of non-classical monocytes.

Suggested Citation

  • Dorothée Selimoglu-Buet & Julie Rivière & Hussein Ghamlouch & Laura Bencheikh & Catherine Lacout & Margot Morabito & M’boyba Diop & Guillaume Meurice & Marie Breckler & Aurélie Chauveau & Camille Debo, 2018. "A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset," Nature Communications, Nature, vol. 9(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:9:y:2018:i:1:d:10.1038_s41467-018-07801-x
    DOI: 10.1038/s41467-018-07801-x
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