期刊
EXPERIMENTAL CELL RESEARCH
卷 321, 期 2, 页码 142-152出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2013.12.001
关键词
MicroRNA; Osteoclastogenesis; TRAF6
资金
- National Natural Science Foundation from China [81170801]
- Hunan provincial natural science foundation from China [13114119]
- Specialized Research Fund for the Doctoral program of High Education from China [20110162110038]
MicroRNAs (miRNAs) play important roles in osteoclastogenesis and bone resorption. In the present study, we found that miR-125a was dramatically down-regulated during macrophage colony stimulating factor (M-CSF) and receptor activator of nuclear factor-kappa B ligand (RANKL) induced osteoclastogenesis of circulating CD14+ peripheral blood mononuclear cells (PBMCs). Overexpression of miR-125a in CD14+ PBMCs inhibited osteoclastogenesis, while inhibition of miR-125a promoted osteoclastogenesis. TNF receptor-associated factor 6 (TRAF6), a transduction factor for RANKL/RANK/NFATcl signal, was confirmed to be a target of miR-125a. EMSA and ChIP assays confirmed that NFATc1 bound to the promoter of the miR-125a. Overexpression of NFATcl inhibited miR-125a transcription, and block of NFATcl expression attenuated RANKL-regulated miR-125a transcription. Here, we reported that miR-125a played a biological function in osteoclastogenesis through a novel TRAF6/ NFATc1/miR-125a regulatory feedback loop. It suggests that regulation of miR-125a expression may be a potential strategy for ameliorating metabolic disease. (C) 2013 Elsevier Inc. All rights reserved.
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