期刊
BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR CELL RESEARCH
卷 1833, 期 8, 页码 1936-1946出版社
ELSEVIER SCIENCE BV
DOI: 10.1016/j.bbamcr.2013.04.007
关键词
Molecular circuitry; Monocyte-macrophage differentiation; MiR-142-3p; Egr2; Chronic myelomonocytic leukemia
资金
- Ligue Contre le Cancer (Conference de coordination inter-departementale, Comite de Saone-et-Loire)
- Conseil Regional de Bourgogne
- ANR
- Ligue Nationale Contre le Cancer
- INCa
- Fondation de France (Comite Leucemie)
- Association Laurette Fugain
- Ministere de l'Enseignement Superieur et de la Recherche of France (MESR)
- Association pour la Recherche sur le Cancer (ARC)
- Societe Francaise d'Hematologie (SFH)
- MESR
- Ligue de Saone-et-Loire contre le Cancer
- ARC
- SFH
- Inserm
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. (C) 2013 Elsevier B.V. All rights reserved.
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