A role for miR-142-3p in colony-stimulating factor 1-induced monocyte differentiation into macrophages

Brice Lagrange, Romain Z. Martin, Nathalie Droin, Romain Aucagne, Jérôme Paggetti, Anne Largeot, Raphaël Itzykson, Eric Solary, Laurent Delva*, Jean Noël Bastie

*Corresponding author for this work

    Research output: Contribution to journalArticleResearchpeer-review

    46 Citations (Scopus)

    Abstract

    The differentiation of human peripheral blood monocytes into macrophages can be reproduced ex vivo by culturing the cells in the presence of colony-stimulating factor 1 (CSF1). Using microarray profiling to explore the role of microRNAs (miRNAs), we identified a dramatic decrease in the expression of the hematopoietic specific miR-142-3p. Up- and down-regulation of this miRNA in primary human monocytes altered CSF1-induced differentiation of monocytes, as demonstrated by changes in the expression of the cell surface markers CD16 and CD163. One of the genes whose expression is repressed by miR-142-3p encodes the transcription factor Early Growth Response 2 (Egr2). In turn, Egr2 associated with its co-repressor NGFI-A (Nerve Growth Factor-Induced gene-A) binding protein 2 (NAB2) binds to the pre-miR-142-3p promoter to negatively regulate its expression. Interestingly, the expression of miR-142-3p is abnormally low in monocytes from patients with the most proliferative forms of chronic myelomonocytic leukemia (CMML), and miR-142-3p re-expression in CMML dysplastic monocytes can improve their differentiation potential. Altogether, miR-142-3p which functions in a molecular circuitry with Egr2 is an actor of CSF1-induced differentiation of human monocytes whose expression could be altered in CMML.

    Original languageEnglish
    Pages (from-to)1936-1946
    Number of pages11
    JournalBiochimica et Biophysica Acta - Molecular Cell Research
    Volume1833
    Issue number8
    DOIs
    Publication statusPublished - Aug 2013

    Keywords

    • Chronic myelomonocytic leukemia
    • Egr2
    • MiR-142-3p
    • Molecular circuitry
    • Monocyte-macrophage differentiation

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