Calycosin Suppresses RANKL-Mediated Osteoclastogenesis through Inhibition of MAPKs and NF-κB

Quan, Gui-Hua; Wang, Hongbing; Cao, Jinjin; Zhang, Yuxin; Wu, Dexi; Peng, Qisheng; Liu, Ning; Sun, Weijia

doi:10.3390/ijms161226179

Cited by 51 publications

(39 citation statements)

References 34 publications

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“…It has been reported that specific genes, such as cathepsin K, MMP-9, and TRAP, are upregulated in response to RANKL [25][26][27]. Our results demonstrated that the expression of these osteoclastspecific genes was increased by RANKL, and IL-35 enhanced such gene expression similarly to other cytokines including IL-17 and IL-15 [28,29].…”

Section: Discussionsupporting

confidence: 60%

IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells

Kamiya

Kikuchi

Goto

et al. 2020

IJMS

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Interleukin (IL)-35 is an immunosuppressive cytokine mainly produced by regulatory T cells. IL-35 mediates immunological functions by suppressing the inflammatory immune response. However, the role of IL-35 in bone-destructive diseases remains unclear, especially in terms of osteoclastogenesis. Therefore, the current study investigated the synergistic effect of IL-35 on osteoclastogenesis that is involved the pathogeneses of periodontitis and rheumatoid arthritis. Osteoclastic differentiation and osteoclastogenesis of RAW264 (RAW) cells induced by receptor activator of nuclear factor (NF)-κB ligand (RANKL) and IL-35 were evaluated by tartrate-resistant acid phosphate staining, hydroxyapatite resorption assays, and quantitative polymerase chain reaction. The effect of IL-35 on RANKL-stimulated signaling pathways was assessed by Western blot analysis. Costimulation of RAW cells by RANKL and IL-35 induced osteoclastogenesis significantly compared with stimulation by RANKL alone. Phosphorylations of extracellular signal-regulated kinase (ERK) and p38 mitogen-activated protein kinase tended to be increased by RANKL and IL-35 compared with RANKL or IL-35 alone. Additionally, the osteoclastogenesis induced by RANKL and IL-35 was suppressed by inhibition of ERK. In this study, IL-35 and RANKL induced osteoclastogenesis synergistically. Previous reports have shown that IL-35 suppresses the differentiation of osteoclasts. Therefore, IL-35 might play dual roles of destruction and protection in osteoclastogenesis.

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Section: Discussionsupporting

confidence: 60%

IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells

Kamiya

Kikuchi

Goto

et al. 2020

IJMS

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“…Calycosin reduced NF‐κB activation in TNF‐α‐stimulated 16HBE cells or LPS‐stimulated human keratinocytes . Calycosin inhibits the phosphorylation of ERK 1/2 and NF‐κB . Hence, calycosin may also regulate the expression of HIF‐1α by transcriptional regulation.…”

Section: Discussionmentioning

confidence: 99%

“…Calycosin, an isoflavonoid phytoestrogen isolated from Astragali Radix, was reported to possess antitumour and anti‐inflammation properties . The dried roots of Astragali Radix, called “Huang Qi” in Chinese, are well known as a basic traditional Chinese medicine for thousands of years.…”

Section: Introductionmentioning

confidence: 99%

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Jia

Wang

et al. 2018

J Cellular Molecular Medi

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Calycosin, a bioactive component derived from Astragali Radix (AR; Huang Qi), has been shown to have an effect of anti‐allergic dermatitis with unknown mechanism. This study aims to investigate the mechanism of calycosin related to tight junctions (TJs) and HIF‐1α both in FITC‐induced mice allergic contact dermatitis and in IL‐1β stimulated HaCaT keratinocytes. Th2 cytokines (IL‐4, IL‐5 and IL‐13) were detected by ELISA. The epithelial TJ proteins (occludin, CLDN1 and ZO‐1), initiative key cytokines (TSLP and IL‐33) and HIF‐1α were assessed by Western blot, real‐time PCR, immunohistochemistry or immunofluorescence. Herein, we have demonstrated that allergic inflammation and the Th2 cytokines in ACD mice were reduced significantly by calycosin treatment. Meanwhile, calycosin obviously decreased the expression of HIF‐1α and repaired TJs both in vivo and in vitro. In HaCaT keratinocytes, we noted that IL‐1β induced the deterioration of TJs, as well as the increased levels of TSLP and IL‐33, which could be reversed by silencing HIF‐1α. In addition, administration of 2‐methoxyestradiolin (2‐ME), a HIF‐1α inhibitor,significantly repaired the TJs and alleviated the allergic inflammation in vivo. Furthermore, TJs were destroyed by DMOG or by overexpressing HIF‐1α in HaCaT keratinocytes, and simultaneously, calycosin down‐regulated the expression of HIF‐1α and repaired the TJs in this process. These results revealed that calycosin may act as a potential anti‐allergy and barrier‐repair agent via regulating HIF‐1α in AD and suggested that HIF‐1α and TJs might be possible therapy targets for allergic dermatitis.

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“…On the fifth day after seeding, the cells were incubated with 5% (vol/vol) NaClO 3 for 5 min at room temperature to remove the cells. As described in the modified Von Kossa method (Quan et al, ; Xu et al, ), 5% (wt/vol) AgNO 3 was added and incubated at room temperature for 1 h in the dark. Subsequently, 10% formaldehyde and 5% (wt/vol) Na 2 CO 3 were added to the cells and incubated at room temperature for 5 min, following which the cells were washed five times with water.…”

Section: Methodsmentioning

confidence: 99%

Tatarinan T, an α‐asarone‐derived lignin, attenuates osteoclastogenesis induced by RANKL via the inhibition of NFATc1/c‐Fos expression

Zhang

Wang

Xie

et al. 2019

Cell Biology International

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We have previously reported that the lignin-like compounds, Tatarinan O (TO) and Tatarinan N (TN), extracted from the roots of Acorus tatarinowii Schott, inhibit receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis. In the present study, the potential function of the α-asarone-derived lignins, Tatarinan T (TT) and Tatarinan A (TA), to regulate RANKL-induced osteoclastogenesis was investigated, and it was found that only early treatment with TT may inhibit RANKL-triggered formation of osteoclasts and resorption. The results revealed repressed expression levels of several osteoclast marker genes, including ATPase H + -transporting V0 subunit d2 (Atp6v0d2), αvβ3 integrin, and osteoclast-associated receptor (OSCAR), following TT treatment during osteoclastogenesis. Moreover, TT reduced the expression levels of the core transcription elements, nuclear factor of activated T-cells cytoplasmic 1 (NFATc1) and c-Fos. However, western blotting analysis showed that TT treatment did not alter nuclear factor-κΒ (NF-κB) activation or mitogen-activated protein kinase (MAPK) or Syk/Btk/phospholipase Cγ2 (PLCγ2) phosphorylation. Taken together, these results suggest the potential of TT in the treatment of diseases of increased bone resorption.

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Calycosin Suppresses RANKL-Mediated Osteoclastogenesis through Inhibition of MAPKs and NF-κB

Cited by 51 publications

References 34 publications

IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells

IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells

Calycosin alleviates allergic contact dermatitis by repairing epithelial tight junctions via down‐regulating HIF‐1α

Tatarinan T, an α‐asarone‐derived lignin, attenuates osteoclastogenesis induced by RANKL via the inhibition of NFATc1/c‐Fos expression

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