Regulation of Osteoclast Differentiation by Cytokine Networks

Amarasekara, Dulshara Sachini; Yun, Hyo In; Kim, Su-Mi; Lee, Nari; Kim, Hyun-Jong; Rho, Jaerang

doi:10.4110/in.2018.18.e8

Cited by 368 publications

(363 citation statements)

References 127 publications

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“…A close relation between bone turnover and the immune system has been previously shown by Ginaldi et al (14). Various proinflammatory cytokines, such as TNF-a and IL-1b, have been associated with increased bone turnover by affecting osteoclast differentiation and function (4,(15)(16)(17).…”

mentioning

confidence: 69%

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The alarmin S100A9 hampers osteoclast differentiation from human circulating precursors by reducing the expression of RANK

Ceglie¹,

Blom²,

Davar

et al. 2019

FASEB j.

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The alarmin S100A8/A9 is implicated in sterile inflammation‐induced bone resorption and has been shown to increase the bone‐resorptive capacity of mature osteoclasts. Here, we investigated the effects of S100A9 on osteoclast differentiation from human CD14+ circulating precursors. Hereto, human CD14+ monocytes were isolated and differentiated toward osteoclasts with M‐CSF and receptor activator of NF‐κB (RANK) ligand (RANKL) in the presence or absence of S100A9. Tartrate‐resistant acid phosphatase staining showed that exposure to S100A9 during monocyte‐to‐osteoclast differentiation strongly decreased the numbers of multinucleated osteoclasts. This was underlined by a decreased resorption of a hydroxyapatite‐like coating. The thus differentiated cells showed a high mRNA and protein production of proinflammatory factors after 16 h of exposure. In contrast, at d 4, the cells showed a decreased production of the osteoclast‐promoting protein TNF‐α. Interestingly, S100A9 exposure during the first 16 h of culture only was sufficient to reduce osteoclastogenesis. Using fluorescently labeled RANKL, we showed that, within this time frame, S100A9 inhibited the M‐CSF‐mediated induction of RANK. Chromatin immunoprecipitation showed that this was associated with changes in various histone marks at the epigenetic level. This S100A9‐induced reduction in RANK was in part recovered by blocking TNF‐α but not IL‐1. Together, our data show that S100A9 impedes monocyte‐to‐osteoclast differentiation, probably via a reduction in RANK expression.—Di Ceglie, I., Blom, A. B., Davar, R., Logie, C., Martens, J. H. A., Habibi, E., Böttcher, L.‐M., Roth, J., Vogl, T., Goodyear, C. S., van der Kraan, P. M., van Lent, P. L., van den Bosch, M. H. The alarmin S100A9 hampers osteoclast differentiation from human circulating precursors by reducing the expression of RANK. FASEB J. 33, 10104–10115 (2019). http://www.fasebj.org

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mentioning

confidence: 69%

“…Both osteoclast differentiation and activation of the resorptive activity are tightly regulated, and therefore, deregulation of these processes, due to hyperinflammation, for example, leads to serious dysfunctioning of the bone tissue (4,5).…”

mentioning

confidence: 99%

The alarmin S100A9 hampers osteoclast differentiation from human circulating precursors by reducing the expression of RANK

Ceglie¹,

Blom²,

Davar

et al. 2019

FASEB j.

View full text Add to dashboard Cite

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“…These signals might regulate ALD hHSC/mHSC activation, motility, and the cross talk between alcohol‐damaged hepatocytes and Kupffer cells/macrophages. Remarkably, a combination of five to six of these genes was associated with astroglial sensome in Alzheimer's disease, amyotrophic lateral sclerosis, and osteoclasts differentiation, outlining the functional commonalities of these genes for disease manifestation in various tissues.…”

Section: Discussionmentioning

confidence: 96%

Primary Alcohol‐Activated Human and Mouse Hepatic Stellate Cells Share Similarities in Gene‐Expression Profiles

et al. 2020

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Alcoholic liver disease (ALD) is a leading cause of cirrhosis in the United States, which is characterized by extensive deposition of extracellular matrix proteins and formation of a fibrous scar. Hepatic stellate cells (HSCs) are the major source of collagen type 1 producing myofibroblasts in ALD fibrosis. However, the mechanism of alcohol‐induced activation of human and mouse HSCs is not fully understood. We compared the gene‐expression profiles of primary cultured human HSCs (hHSCs) isolated from patients with ALD (n = 3) or without underlying liver disease (n = 4) using RNA‐sequencing analysis. Furthermore, the gene‐expression profile of ALD hHSCs was compared with that of alcohol‐activated mHSCs (isolated from intragastric alcohol‐fed mice) or CCl4‐activated mouse HSCs (mHSCs). Comparative transcriptome analysis revealed that ALD hHSCs, in addition to alcohol‐activated and CCl4‐activated mHSCs, share the expression of common HSC activation (Col1a1 [collagen type I alpha 1 chain], Acta1 [actin alpha 1, skeletal muscle], PAI1 [plasminogen activator inhibitor‐1], TIMP1 [tissue inhibitor of metalloproteinase 1], and LOXL2 [lysyl oxidase homolog 2]), indicating that a common mechanism underlies the activation of human and mouse HSCs. Furthermore, alcohol‐activated mHSCs most closely recapitulate the gene‐expression profile of ALD hHSCs. We identified the genes that are similarly and uniquely up‐regulated in primary cultured alcohol‐activated hHSCs and freshly isolated mHSCs, which include CSF1R (macrophage colony‐stimulating factor 1 receptor), PLEK (pleckstrin), LAPTM5 (lysosmal‐associated transmembrane protein 5), CD74 (class I transactivator, the invariant chain), CD53, MMP9 (matrix metallopeptidase 9), CD14, CTSS (cathepsin S), TYROBP (TYRO protein tyrosine kinase‐binding protein), and ITGB2 (integrin beta‐2), and other genes (compared with CCl4‐activated mHSCs). Conclusion: We identified genes in alcohol‐activated mHSCs from intragastric alcohol‐fed mice that are largely consistent with the gene‐expression profile of primary cultured hHSCs from patients with ALD. These genes are unique to alcohol‐induced HSC activation in two species, and therefore may become targets or readout for antifibrotic therapy in experimental models of ALD.

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“…[38][39][40] IL-6 is a potential inducer of the osteoclast differentiation independent of RANKL and IL-6 receptor inhibition results in the blockage of the osteoclast formation both in vitro and in vivo. [41][42][43] Thus, inhibition of inflammation represents a promising therapeutic approach to treated wear debris-induced inflammatory osteolysis. 44 In the present study, our results suggested that the inhibition of pro-inflammatory cytokines by an H 2 S donor markedly decreased the presence of osteoclasts in murine models.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide protects against particle‐induced inflammatory response and osteolysis via SIRT1 pathway in prosthesis loosening

et al. 2020

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Wear debris‐induced osteolysis and ensuing aseptic loosening is the main cause of implant failure and revision surgery. Wear debris‐induced inflammatory response plays key roles in peri‐implant osteolysis. Recently, substantial of evidence suggests that hydrogen sulfide (H2S), the third gasotransmitter, is a critical player regulating inflammation. However, the role and therapeutic potential of H2S in wear debris‐induced inflammation and osteolysis remains to be defined. In the present study, we investigated the effect of H2S on wear debris‐induced pro‐inflammatory cytokines expression and osteolysis in vitro and in vivo. With a slow‐releasing H2S donor GYY4137, our study demonstrated that H2S attenuated wear debris‐induced osteolysis and osteoclastogenesis in murine calvaria resorption models. The expression of tumor necrosis factor‐alpha (TNF‐α), interleukin‐1β (IL‐1β), and interleukin‐6 (IL‐6) that stimulated by wear particles were significantly reduced by GYY4137. Further, the level of sirtuin 1 (SIRT1), which possesses anti‐inflammation property, was examined in vivo and in macrophages. And we found that wear debris decreased the expression of SIRT1. Cotreated macrophages with GYY4137 in part reversed the decline of SIRT1. More importantly, with the SIRT1 recombinant lentivirus and small interfering RNAs (siRNA) against SIRT1, our data indicated that SIRT1 mediated the inhibitory effects of GYY4137 on wear debris‐induced inflammation. Collectively, these results suggested that exogenous H2S production (via H2S donors) may represent a potential approach for the treatment of wear particle‐induced osteolysis.

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Regulation of Osteoclast Differentiation by Cytokine Networks

Cited by 368 publications

References 127 publications

The alarmin S100A9 hampers osteoclast differentiation from human circulating precursors by reducing the expression of RANK

The alarmin S100A9 hampers osteoclast differentiation from human circulating precursors by reducing the expression of RANK

Primary Alcohol‐Activated Human and Mouse Hepatic Stellate Cells Share Similarities in Gene‐Expression Profiles

Hydrogen sulfide protects against particle‐induced inflammatory response and osteolysis via SIRT1 pathway in prosthesis loosening

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