Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

Zhu, Xiaojuan; Zhao, Yinghua; Jiang, Yuxue; Qin, Tianxue; Chen, Jintong; Chu, Xiao; Yi, Qing; Gao, Sujun; Wang, Siqing

doi:10.18632/oncotarget.18411

Cited by 21 publications

(20 citation statements)

References 34 publications

(48 reference statements)

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“…Similarly, other evidence shows a suppressive effect of IL-33 on osteoclast differentiation via the inactivation of a key regulator of RANKL-induced osteoclast formation, the nuclear factor of activated T-cell cytoplasmic 1 [107]. Moreover, experimental studies suggest that mice missing the IL-33 receptor show a low bone mass and an increase in osteoclast formation [108].…”

Section: Il-33mentioning

confidence: 91%

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

et al. 2020

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Alarmins are endogenous mediators released by cells following insults or cell death to alert the host’s innate immune system of a situation of danger or harm. Many of these, such as high-mobility group box-1 and 2 (HMGB1, HMGB2) and S100 (calgranulin proteins), act through RAGE (receptor for advanced glycation end products), whereas the IL-1 and IL-33 cytokines bind the IL-1 receptors type I and II, and the cellular receptor ST2, respectively. The alarmin family and their signal pathways share many similarities of cellular and tissue localization, functions, and involvement in various physiological processes and inflammatory diseases including osteoporosis. The aim of the review was to evaluate the role of alarmins in osteoporosis. A bibliographic search of the published scientific literature regarding the role of alarmins in osteoporosis was organized independently by two researchers in the following scientific databases: Pubmed, Scopus, and Web of Science. The keywords used were combined as follows: “alarmins and osteoporosis”, “RAGE and osteoporosis”, “HMGB1 and osteoporosis”, “IL-1 and osteoporosis”, “IL 33 and osteopororsis”, “S100s protein and osteoporosis”. The information was summarized and organized in the present review. We highlight the emerging roles of alarmins in various bone remodeling processes involved in the onset and development of osteoporosis, as well as their potential role as biomarkers of osteoporosis severity and progression. Findings of the research suggest a potential use of alarmins as pharmacological targets in future therapeutic strategies aimed at preventing bone loss and fragility fractures induced by aging and inflammatory diseases.

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Section: Il-33mentioning

confidence: 91%

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

et al. 2020

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“…Actin ring formation assays and resorption assays were performed as previously described [ 38 , 39 ]. Pre-osteoclasts were seeded on bone slices in 96-well plates at a density of 8 × 10 3 cells/well with three replicates for 5–7 days.…”

Section: Methodsmentioning

confidence: 99%

Paeoniflorin regulates osteoclastogenesis and osteoblastogenesis via manipulating NF-κB signaling pathway bothin vitroandin vivo

et al. 2017

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The metabolic balance between synthesis and resorption of the bone is maintained by osteoblasts and osteoclasts, respectively. Identification of agents that stimulate bone formation and suppress excessive osteoclast formation, may aid in preventing and treating conditions like osteoporosis and periprosthetic loosening. Paeoniflorin is a natural product derived from Paeonia lactiflora Pall with anti-inflammatory, analgesic, and diuretic properties. However, the effect of paeoniflorin on osteoclastogenesis and osteoblastogenesis is unknown. Herein, we demonstrated that paeoniflorin has a dose-dependent suppressive action on RANKL-evoked osteoclast differentiation and bone resorption, achieved by inhibiting the NF-κB pathway and subunit p65 nuclear translocation. Simultaneously, paeoniflorin was also found to stimulate osteoblast differentiation and bone mineralization, in addition to rescuing TNFα-impaired osteoblastogenesis. At the molecular level, paeoniflorin was found to inhibit NF-κB transcriptional activity and stimulate osteoblastogenesis-related marker gene expression (ALP, osteocalcin, OPN and Runx2), a trend that was inhibited by p65 overexpression. In ovariectomized mice, paeoniflorin was found to improve osteoblast activity, inhibit osteoclast activity, and thus, reduce ovariectomy-induced osteoporosis. Our study demonstrated that paeoniflorin simultaneously suppressed osteoclastogenesis and facilitated osteoblastogenesis by manipulating the actions of NF-κB. Therefore, paeoniflorin may serve as an ideal therapeutic antidote for osteoporosis.

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“…IL-33 is a member of the IL-1 family and functions as an important bone-protecting cytokine. IL-33/ST2 signaling reduces bone loss, inhibits osteoclast formation, promotes osteoblast function, interferes with the production of RANKL and macrophage colony-stimulating factor, and decreases NFATc1 expression in osteoclast precursors [32,33]. In this study, the serum concentrations of IL-1, IL-7, and TNF-α were increased and those of IL-33 were decreased in mice with Dex-induced OP compared with healthy control mice, and all of these changes were reversed to the normal state by the sevenweek YSBGY treatment.…”

Section: Discussionmentioning

confidence: 99%

The Antiosteoporosis Effects of Yishen Bugu Ye Based on Its Regulation on the Differentiation of Osteoblast and Osteoclast

Zhang

Meng

et al. 2020

BioMed Research International

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Yishen Bugu Ye (YSBGY), a traditional Chinese medicine comprising 12 types of medicinal herbs, is often prescribed in China to increase bone strength. In this study, the antiosteoporotic effects of YSBGY were investigated in C57BL/6 mice afflicted with dexamethasone-(Dex-) induced osteoporosis (OP). The results showed that YSBGY reduced the interstitial edema in the liver and kidney of mice with Dex-induced OP. It also increased the number of trabecular bone elements and chondrocytes in the femur, promoted cortical bone thickness and trabecular bone density, and modulated the OP-related indexes in the femur and tibia of OP mice. It also increased the serum concentrations of type I collagen, osteocalcin, osteopontin, bone morphogenetic protein-2, bone morphogenetic protein receptor type 2, C-terminal telopeptide of type I collagen, and runt-related transcription factor-2 and reduced those of tartrate-resistant acid phosphatase 5 and nuclear factor of activated T cells in these mice, suggesting that it improved osteoblast differentiation and suppressed osteoclast differentiation. The anti-inflammatory effect of YSBGY was confirmed by the increase in the serum concentrations of interleukin-(IL-) 33 and the decrease in concentrations of IL-1, IL-7, and tumor necrosis factor-α in OP mice. Furthermore, YSBGY enhanced the serum concentrations of superoxide dismutase and catalase in these mice, indicating that it also exerted antioxidative effects. This is the first study to confirm the antiosteoporotic effects of YSBGY in mice with Dex-induced OP, and it showed that these effects may be related to the YSBGYinduced modulation of the osteoblast/osteoclast balance and serum concentrations of inflammatory factors. These results provide experimental evidence supporting the use of YSBGY for supporting bone formation in the clinical setting.

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Dectin-1 signaling inhibits osteoclastogenesis via IL-33-induced inhibition of NFATc1

Cited by 21 publications

References 34 publications

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

Alarmins in Osteoporosis, RAGE, IL-1, and IL-33 Pathways: A Literature Review

Paeoniflorin regulates osteoclastogenesis and osteoblastogenesis via manipulating NF-κB signaling pathway bothin vitroandin vivo

The Antiosteoporosis Effects of Yishen Bugu Ye Based on Its Regulation on the Differentiation of Osteoblast and Osteoclast

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