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MafB negatively regulates RANKL-mediated osteoclast differentiation

Title
MafB negatively regulates RANKL-mediated osteoclast differentiation
Authors
Kim K.Jung H.K.Lee J.Hye M.J.Kook H.Kyung K.K.Soo Y.L.Kim N.
Ewha Authors
이수영
SCOPUS Author ID
이수영scopus
Issue Date
2007
Journal Title
Blood
ISSN
0006-4971JCR Link
Citation
vol. 109, no. 8, pp. 3253 - 3259
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Receptor activator of nuclear factor κB ligand (RANKL) induces osteoclast formation from hematopoietic cells via regulation of various transcription factors. Here, we show that MafB negatively regulates RANKL-induced osteoclast differentiation. Expression levels of MafB are significantly reduced by RANKL during osteoclastogenesis. Overexpression of MafB in bone marrow-derived monocyte/macrophage lineage cells (BMMs) inhibits the formation of TRAP+ multinuclear osteoclasts, but phagocytic activity of BMMs is retained. Furthermore, overexpression of MafB in BMMs attenuates the gene induction of NFATc1 and osteoclast-associated receptor (OSCAR) during RANKL-mediated osteoclastogenesis. In addition, MafB proteins interfere with the DNA-binding ability of c-Fos, Mitf, and NFATc1, inhibiting their transactivation of NFATc1 and OSCAR. Furthermore, reduced expression of MafB by RNAi enhances osteoclastogenesis and increases expression of NFATc1 and OSCAR. Taken together, our results suggest that MafB can act as an important modulator of RANKL-mediated osteoclastogenesis. © 2007 by The American Society of Hematology.
DOI
10.1182/blood-2006-09-048249
Appears in Collections:
자연과학대학 > 생명과학전공 > Journal papers
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