Regulation of Receptor Activator of NF-κB Ligand-induced Osteoclastogenesis by Endogenous Interferon-β (INF-β) and Suppressors of Cytokine Signaling (SOCS)

Hayashi, Toshikichi; Kaneda, Toshio; Toyama, Yoshiaki; Kumegawa, Masayoshi; Hakeda, Yoshiyuki

doi:10.1074/jbc.m203836200

Cited by 90 publications

(74 citation statements)

References 62 publications

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“…[49][50][51] The continuous production of IFN-b by injection of IFN-b-expressing fibroblast or daily subcutaneous treatment with recombinant IFN-b inhibited inflammation as well as bone destruction in a system of collagen-induced arthritis in mice. 52,53 In addition, the expression of IFN-b was increased in synovial tissue of patients with RA.…”

Section: Discussionmentioning

confidence: 99%

A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats

Kukita

Teramachi

et al. 2009

Laboratory Investigation

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Galectin-3 is a b-galactoside-binding animal lectin having pleiotropic effects on cell growth, differentiation, and apoptosis. This lectin has been shown to be involved in phagocytosis by macrophages and in inflammation. Here we investigated an involvement of galectin-3 in the regulatory process of inflammatory bone resorption in rats with adjuvant-induced arthritis (AA rats) accompanying severe bone destruction in the ankle joints. The protein level of galectin-3 in the ankle-joint extracts was markedly augmented at week 3 after adjuvant injection, at the time when severe bone destruction was observed. Immunohistochemical analysis revealed an extremely high expression of galectin-3 in macrophages and granulocytes infiltrated in the area of severe bone destruction. To estimate the role of galectin-3 in osteoclastogenesis and osteoclastic bone resorption, recombinant galectin-3 was added to in vitro culture systems. Galectin-3 markedly inhibited the formation of osteoclasts in cultures of murine osteoclast precursor cell line as well as in rat bone marrow culture systems. This inhibition was not observed by heat-inactivated galectin-3 or by galectin-7. Although recombinant galectin-3 did not affect signaling through mitogen-activated protein kinase (MAPK) or nuclear factor-kB (NF-kB), it specifically suppressed the induction of nuclear factor of activated T-cells c1 (NFATc1). Galectin-3 significantly inhibited dentine resorption by mature osteoclasts in vitro. Furthermore, in vivo studies clearly showed a significant suppression of bone destruction and osteoclast recruitment accompanying arthritis, when galectin-3 was injected into the cavity of ankle joint of AA rats. Thus, abundant galectin-3 observed in the area of severe bone destruction may act as a negative regulator for the upregulated osteoclastogenesis accompanying inflammation to prevent excess bone destruction.

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Section: Discussionmentioning

confidence: 99%

A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats

Kukita

Teramachi

et al. 2009

Laboratory Investigation

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“…Because FliC is reported to activate the NF-kB pathway in epithelial cells Reed et al, 2002;Takahashi et al, 2001) and because the NF-kB pathway participates in the induction of SOCS-3 expression (Hayashi et al, 2002), we investigated the participation of the NF-kB signalling pathway in SPI-2-dependent expression of SOCS-3. As shown in Fig.…”

Section: Detection Of Flic In Salmonella-infected Macrophagesmentioning

confidence: 99%

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Uchiya

Nikai

2008

Microbiology

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“…It has also been shown that RANKL induces the interferon-β gene in OCL precursor cells, and that IFN-β inhibits OCL differentiation by interfering with the RANKL induced expression of c-fos to maintain bone homeostasis (Takayanagi et al, 2002). However, RANKL treatment also induces suppressors of cytokine signaling, SOCS-1 and 3 which suppress IFN signaling in OCL precursors counteracting IFN-β intrinsic inhibition of OCL development (Hayashi et al, 2002). Therefore, it is important to delineate the molecular mechanisms by which IFN-γ regulate gene expression in OCL precursor cells.…”

Section: Discussionmentioning

confidence: 99%

Functional characterization of human osteoclast inhibitory peptide-1 (OIP-1/hSca) gene promoter

Shanmugarajan

Ito

Kajiya

et al. 2006

Gene

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We have recently identified and characterized the human osteoclast (OCL) inhibitory peptide-1 (OIP-1/hSca), a member of Ly-6 gene family. OIP-1 is an important physiologic regulator of OCL development and bone resorption activity. To determine the molecular mechanisms that regulate OIP-1 gene expression in OCL precursor cells, we isolated and characterized the OIP-1/hSca gene (2 Kb) promoter sequence. IFN-γ (50 ng/ml) treatment of RAW 264.7 macrophage cells transfected with OIP-1 gene (−1 to −1988 bp relative to transcription start site) promoter-luciferase reporter plasmid demonstrated a significant (4 fold) increase in OIP-1 gene promoter activity. Sequence analysis of OIP-1 gene promoter region further identified a potential Stat-1 binding motif at −1629 to −1639 bp position. Stat-1 specific inhibitor, fludarabine (50 µM) abolished IFN-γ stimulated OIP-1 gene promoter activity. Electrophoretic mobility shift assay (EMSA) further confirmed activated Stat-1 binding to the OIP-1 gene promoter sequence suggesting that IFN-γ regulates OIP-1 gene expression in OCL precursor cells through a Stat-1 dependent signaling pathway. We further show that knock-down of TRADD enhances IFN-γ signaling to increase OIP-1 gene expression in OCL precursor cells. These results should provide insights into the molecular control of OIP-1 gene expression and inhibition of OCL activity in the bone microenvironment

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Regulation of Receptor Activator of NF-κB Ligand-induced Osteoclastogenesis by Endogenous Interferon-β (INF-β) and Suppressors of Cytokine Signaling (SOCS)

Cited by 90 publications

References 62 publications

A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats

A possible suppressive role of galectin-3 in upregulated osteoclastogenesis accompanying adjuvant-induced arthritis in rats

Salmonella virulence factor SpiC is involved in expression of flagellin protein and mediates activation of the signal transduction pathways in macrophages

Functional characterization of human osteoclast inhibitory peptide-1 (OIP-1/hSca) gene promoter

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