Tumor necrosis factor‐α mediates RANK ligand stimulation of osteoclast differentiation by an autocrine mechanism†

Zou, Wei; Hakim, Imad; Tschoep, Katharina; Endres, Stefan; Bar‐Shavit, Zvi

doi:10.1002/jcb.1202

Cited by 127 publications

(129 citation statements)

References 61 publications

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“…LPS is well known to elicit TNF-α (Abu-Amer et al 1997;Zou and Bar-Shavit 2002;Itoh et al 2003), IL-6 (Itoh et al 2003;Sato et al 2004), IL-1α (Hong et al 2004), andIL-1β (Itoh et al 2003) release from monocytes. It is also well established that these cytokines promote Oc formation (Jimi et al 1999;Azuma et al 2000;Zhang et al 2001;Zou et al 2001;Kudo et al 2003;Wei et al 2005). We have confirmed their pro-osteoclastogenic properties but also shown for the first time that these cytokines are released by RANKL-primed pOcs autonomously when exposed to LPS (Fig.…”

Section: Figsupporting

confidence: 80%

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Lipopolysaccharide-Induced Osteoclastogenesis from Mononuclear Precursors: A Mechanism for Osteolysis in Chronic Otitis

Nason

Jung

Chole

2009

JARO

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Osteoclasts are the only cells capable of carrying out bone resorption and therefore are responsible for the osteolysis seen in infectious diseases such as chronic otitis media and infected cholesteatoma. Pseudomonas aeruginosa is the most common organism isolated from these infectious middle ear diseases. In this study, we examined the mechanisms by which P. aeruginosa lipopolysaccharide (LPS) stimulates osteoclastogenesis directly from mononuclear osteoclast precursor cells. Osteoclast precursors demonstrated robust, bone-resorbing osteoclast formation when stimulated by P. aeruginosa LPS only if previously primed with permissive, sub-osteoclastogenic doses of receptor activator of NF-κB ligand (RANKL), suggesting that LPS is osteoclastogenic only during a specific developmental window. Numerous LPS-elicited cytokines were found to be released by osteoclast precursors undergoing P. aeruginosa LPS-mediated osteoclast formation. Two lines of evidence suggest that several cytokines promote Oc formation in an autocrine/paracrine manner. First, inhibition of several cytokine pathways including TNF-α, IL-1, and IL-6 block the osteoclastogenesis induced by LPS. Secondly, increased expression of the receptors for TNF-α and IL-1 was demonstrated by real-time quantitative polymerase chain reaction. Such a mechanism has not previously been established and demonstrates the ability of osteoclast precursors to autonomously facilitate bone destruction.

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Section: Figsupporting

confidence: 80%

“…It also contrasts an in vitro study using Balb/c and C57 mice that revealed TNFR1 but not TNFR2 dependence (Zou et al 2001). Interestingly, the latter study demonstrated that LPS induced release of TNF-α which then promoted Oc formation FIG.…”

Section: Figmentioning

confidence: 70%

Lipopolysaccharide-Induced Osteoclastogenesis from Mononuclear Precursors: A Mechanism for Osteolysis in Chronic Otitis

Nason

Jung

Chole

2009

JARO

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“…For example, a minuscule amount of RANKL is sufficient to synergize with TNF-a to promote osteoclastogenesis from precursor cells. 17,41,47 Figure 5 DcR3-induced osteoclast formation is dependent on ERK and p38 MAPK activation. RAW264.7 cells (a) and human monocytes (b) were pretreated with vehicle, 50 mM PD98059, 1 mM U0126, or 1 mM SB203580 for 20 min prior to stimulation with DcR3 (3 mg/ml), M-CSF, or RANKL.…”

Section: Discussionmentioning

confidence: 99%

Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

Yang

Wang

Hsieh³

et al. 2004

Cell Death Differ

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Recent evidence indicates that the decoy receptor 3 (DcR3) of the TNF receptor superfamily, which initially though prevents cytokine responses of FasL, LIGHT and TL1A by binding and neutralization, can modulate monocyte function through reverse signaling. We show in this work that DcR3 can induce osteoclast formation from human monocytes, murine RAW264.7 macrophages, and bone marrow cells. DcR3-differentiated cells exhibit characteristics unique for osteoclasts, including polynuclear giant morphology, bone resorption, TRAP, CD51/61, and MMP-9 expression. Consistent with the abrogation of osteoclastogenic effect of DcR3 by TNFRFc, DcR3 treatment can induce osteoclastogenic cytokine TNF-a release through ERK and p38 MAPK signaling pathways. We conclude that DcR3 via coupling reverse signaling of ERK and p38 MAPK and stimulating TNF-a synthesis is a critical regulator of osteoclast formation. This action of DcR3 might play an important role in significant osteoclastic activity in osteolytic bone metastases.

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“…Additionally, our previous study showed that EGCG reduces the interleukin-6 synthesis by platelet-derived growth factor without affecting the p70 S6 kinase activation (26). It is generally recognized that platelet-derived growth factor receptor has an intrinsic protein tyrosine kinase activity, whereas TNF-α receptor belongs to the cytokine receptor superfamily, and that the signal transduction mechanisms are quite different from each other (12,27). Thus, it appears likely that different and rather opposite effects of EGCG on p70 S6 kinase activation and interleukin-6 synthesis induced by TNF-α or PDGF-BB in osteoblast-like MC3T3-E1 cells are due to the difference between each receptor-mediated intracellular signaling.…”

Section: Discussionmentioning

confidence: 99%

“…With regard to bone metabolism, TNF-α stimulates the activation of RANK in osteoclasts through RANK ligand expression in osteoblasts, which acts as a potent stimulator of osteoclastogenesis (12). It has been reported that TNF-α stimulates the synthesis of interleukin-6 (13).…”

Section: Introductionmentioning

confidence: 99%

Amplification by (-)-epigallocatechin gallate and chlorogenic acid of TNF-α-stimulated interleukin-6 synthesis in osteoblasts

Yamamoto¹,

Tokuda²,

Kuroyanagi³

et al. 2015

International Journal of Molecular Medicine

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Abstract. Polyphenolic compounds in foods and beverages have beneficial effects on human health. (-)-Epigallocatechin gallate (EGCG) and chlorogenic acid (CGA), a major flavonoid in green tea and a major phenolic acid in coffee, respectively, have potent properties, including antioxidative effects. Our previous study demonstrated that p70 S6 kinase acts as a negative regulator in tumor necrosis factor-α (TNF-α)-stimulated interleukin-6 synthesis in osteoblast-like MC3T3-E1 cells. In the present study, the effects of EGCG and CGA on the TNF-α-stimulated interleukin-6 synthesis were investigated in MC3T3-E1 cells. EGCG and CGA significantly enhanced TNF-α-stimulated interleukin-6 release. In addition, the interleukin-6 mRNA expression levels induced by TNF-α were supported by EGCG, as well as CGA. EGCG markedly attenuated the TNF-α-induced phosphorylation of p70 S6 kinase whereas CGA failed to affect the phosphorylation. These results strongly suggest that EGCG and CGA enhance the TNF-α-stimulated interleukin-6 synthesis in osteoblasts, and that the amplifying effect of EGCG, but not CGA, is exerted via inhibiting p70 S6 kinase.

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Tumor necrosis factor‐α mediates RANK ligand stimulation of osteoclast differentiation by an autocrine mechanism†

Cited by 127 publications

References 61 publications

Lipopolysaccharide-Induced Osteoclastogenesis from Mononuclear Precursors: A Mechanism for Osteolysis in Chronic Otitis

Lipopolysaccharide-Induced Osteoclastogenesis from Mononuclear Precursors: A Mechanism for Osteolysis in Chronic Otitis

Decoy receptor 3 (DcR3) induces osteoclast formation from monocyte/macrophage lineage precursor cells

Amplification by (-)-epigallocatechin gallate and chlorogenic acid of TNF-α-stimulated interleukin-6 synthesis in osteoblasts

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