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

Dorothée Selimoglu-Buet; Julie Rivière; Hussein Ghamlouch; Laura Bencheikh; Catherine Lacout; Margot Morabito; M’boyba Diop; Guillaume Meurice; Marie Breckler; Aurélie Chauveau; Camille Debord; Franck Debeurme; Raphael Itzykson; Nicolas Chapuis; Christophe Willekens; Orianne Wagner-Ballon; Olivier A. Bernard; Nathalie Droin; Eric Solary

doi:10.1038/s41467-018-07801-x

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

Dorothée Selimoglu-Buet, Julie Rivière, Hussein Ghamlouch, Laura Bencheikh, Catherine Lacout, Margot Morabito, M’boyba Diop, Guillaume Meurice, Marie Breckler, Aurélie Chauveau, Camille Debord, Franck Debeurme, Raphael Itzykson, Nicolas Chapuis, Christophe Willekens, Orianne Wagner-Ballon, Olivier A. Bernard, Nathalie Droin, Eric Solary

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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.

Original language	English
Article number	5455
Journal	Nature Communications
Volume	9
Issue number	1
DOIs	https://doi.org/10.1038/s41467-018-07801-x
Publication status	Published - 1 Dec 2018

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Selimoglu-Buet, D., Rivière, J., Ghamlouch, H., Bencheikh, L., Lacout, C., Morabito, M., Diop, M., Meurice, G., Breckler, M., Chauveau, A., Debord, C., Debeurme, F., Itzykson, R., Chapuis, N., Willekens, C., Wagner-Ballon, O., Bernard, O. A., Droin, N., & Solary, E. (2018). A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset. Nature Communications, 9(1), Article 5455. https://doi.org/10.1038/s41467-018-07801-x

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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.",

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Selimoglu-Buet, D, Rivière, J, Ghamlouch, H, Bencheikh, L, Lacout, C, Morabito, M, Diop, M, Meurice, G, Breckler, M, Chauveau, A, Debord, C, Debeurme, F, Itzykson, R, Chapuis, N, Willekens, C, Wagner-Ballon, O, Bernard, OA, Droin, N & Solary, E 2018, 'A miR-150/TET3 pathway regulates the generation of mouse and human non-classical monocyte subset', Nature Communications, vol. 9, no. 1, 5455. https://doi.org/10.1038/s41467-018-07801-x

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AU - Selimoglu-Buet, Dorothée

AU - Rivière, Julie

AU - Ghamlouch, Hussein

AU - Bencheikh, Laura

AU - Lacout, Catherine

AU - Morabito, Margot

AU - Diop, M’boyba

AU - Meurice, Guillaume

AU - Breckler, Marie

AU - Chauveau, Aurélie

AU - Debord, Camille

AU - Debeurme, Franck

AU - Itzykson, Raphael

AU - Chapuis, Nicolas

AU - Willekens, Christophe

AU - Wagner-Ballon, Orianne

AU - Bernard, Olivier A.

AU - Droin, Nathalie

AU - Solary, Eric

PY - 2018/12/1

Y1 - 2018/12/1

N2 - 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.

AB - 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.

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

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