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Id helix-loop-helix proteins negatively regulate TRANCE-mediated osteoclast differentiation

Title
Id helix-loop-helix proteins negatively regulate TRANCE-mediated osteoclast differentiation
Authors
Lee, JKim, KKim, JHJin, HMChoi, HKLee, SHKook, HKim, KKYokota, YLee, SYChoi, YKim, N
Ewha Authors
이수영
SCOPUS Author ID
이수영scopus
Issue Date
2006
Journal Title
BLOOD
ISSN
0006-4971JCR Link
Citation
vol. 107, no. 7, pp. 2686 - 2693
Publisher
AMER SOC HEMATOLOGY
Indexed
SCI; SCIE; SCOPUS WOS
Abstract
Tumor necrosis factor (TNF)-related activation-induced cytokine (TRANCE) induces osteoclast formation from monocyte/macrophage lineage cells via various transcription factors, including the Mi transcription factor (Miff). Here, we show that inhibitors of differentiation/DNA binding (ids), helix-loop-helix (HLH) transcription factors, negatively regulate TRANCE-induced osteoclast differentiation. Expression levels of Id1, Id2, and Id3 genes are significantly reduced by TRANCE during osteoclastogenesis. Interestingly, overexpression of the 3 Id genes in bone marrow-derived monocyte( macrophage lineage cells (BMMs) inhibits the formation of tartrate-resistant acid phosphatase (TRAP)-positive multinuclear osteoclasts, but it does not alter the ability of BMMs to either phagocytose or differentiate into dendritic cells (DCs). Overexpression of Id2 in BMMs attenuates the gene induction of nuclear factor of activated T cells cl (NFATc1) and osteoclast-associated receptor (OSCAR) during TRANCE-mediated osteoclastogenesis. Furthermore, Id proteins interact with Miff, a basic HLH (bHLH) transcription factor, and inhibit its transactivation of OSCAR, which is a costimulatory receptor expressed by osteoclast precursors, by attenuating the DNA binding ability of Mitf to the E-box site of the OSCAR promoter. Taken together, our results reveal both a new facet of negative regulation, mediated by Id proteins, as well as the mechanism whereby TRANCE signaling overcomes it, allowing osteoclastogenesis to proceed.
DOI
10.1182/blood-2005-07-2798
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자연과학대학 > 생명과학전공 > Journal papers
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