| Literature DB >> 30575719 |
Dorothée Selimoglu-Buet1, Julie Rivière2,3, Hussein Ghamlouch2,3, Laura Bencheikh2,3, Catherine Lacout2,3, Margot Morabito2,3, M'boyba Diop4, Guillaume Meurice4, Marie Breckler4, Aurélie Chauveau2,5, Camille Debord2,6, Franck Debeurme2,3, Raphael Itzykson2,7, Nicolas Chapuis8, Christophe Willekens2,9,10, Orianne Wagner-Ballon11, Olivier A Bernard2,3, Nathalie Droin2,3,4, Eric Solary12,13,14.
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.Entities:
Mesh：
Substances：
Year: 2018 PMID： 30575719 PMCID： PMC6303340 DOI： 10.1038/s41467-018-07801-x
Source DB: PubMed Journal: Nat Commun ISSN： 2041-1723 Impact factor: 14.919