Erucin inhibits osteoclast formation via suppressing cell–cell fusion molecule DC-STAMP without influencing mineralization by osteoblasts

Takagi, Tetsuya; Inoue, Hirofumi; Fujii, Shungo; Takahashi, Nobuyuki; Uehara, Mariko

doi:10.1186/s13104-022-05988-3

Cited by 5 publications

(2 citation statements)

References 19 publications

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“…Secreted osteoclastogenic factor of activated T cells (SOFAT) is produced by activated T cells and stimulates bone resorption in the absence of osteoblasts or RANKL ( 33 ). Dendritic cell-specific transmembrane protein (DC-STAMP) plays an essential role in the formation of multinucleated osteoclasts ( 34 , 35 ). Knock-down of DC-STAMP abrogates cell–cell fusion.…”

Section: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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Periodontitis involves the loss of connective tissue attachment and alveolar bone. Single cell RNA-seq experiments have provided new insight into how resident cells and infiltrating immune cells function in response to bacterial challenge in periodontal tissues. Periodontal disease is induced by a combined innate and adaptive immune response to bacterial dysbiosis that is initiated by resident cells including epithelial cells and fibroblasts, which recruit immune cells. Chemokines and cytokines stimulate recruitment of osteoclast precursors and osteoclastogenesis in response to TNF, IL-1β, IL-6, IL-17, RANKL and other factors. Inflammation also suppresses coupled bone formation to limit repair of osteolytic lesions. Bone lining cells, osteocytes and periodontal ligament cells play a key role in both processes. The periodontal ligament contains cells that exhibit similarities to tendon cells, osteoblast-lineage cells and mesenchymal stem cells. Bone lining cells consisting of mesenchymal stem cells, osteoprogenitors and osteoblasts are influenced by osteocytes and stimulate formation of osteoclast precursors through MCSF and RANKL, which directly induce osteoclastogenesis. Following bone resorption, factors are released from resorbed bone matrix and by osteoclasts and osteal macrophages that recruit osteoblast precursors to the resorbed bone surface. Osteoblast differentiation and coupled bone formation are regulated by multiple signaling pathways including Wnt, Notch, FGF, IGF-1, BMP, and Hedgehog pathways. Diabetes, cigarette smoking and aging enhance the pathologic processes to increase bone resorption and inhibit coupled bone formation to accelerate bone loss. Other bone pathologies such as rheumatoid arthritis, post-menopausal osteoporosis and bone unloading/disuse also affect osteoblast lineage cells and participate in formation of osteolytic lesions by promoting bone resorption and inhibiting coupled bone formation. Thus, periodontitis involves the activation of an inflammatory response that involves a large number of cells to stimulate bone resorption and limit osseous repair processes.

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Section: Osteoblasts Osteocytes Periodontal Ligament and Osteoclast C...mentioning

confidence: 99%

Impact of the host response and osteoblast lineage cells on periodontal disease

Zhou

Graves²

2022

Front. Immunol.

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“…However, prolonged use of these agents may cause side effects leading to drug discontinuation, which highlights the need for a safe, efficacious alternative (Zhang et al, 2023). Recently, numerous herbal extracts have been researched as potential anti-osteoporosis therapeutic options owing to their potent effects and few side effects (Takagi et al, 2022;Zheng et al, 2022;Xu et al, 2023). This study presents novel findings showing that NBP suppresses osteoclast differentiation and bone resorption in vitro through reducing RANKL-induced ROS levels and blocking the MAPK signaling pathway.…”

Section: Discussionmentioning

confidence: 83%

Unveiling the potential of Butylphthalide: inhibiting osteoclastogenesis and preventing bone loss

Yanbin,

Yilin,

Yaomin

et al. 2024

Front. Pharmacol.

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Osteoporosis, resulting from overactive osteoclasts and leading to elevated fracture risk, has emerged as a global public health concern due to the aging population. Therefore, inhibiting osteoclastogenesis and bone resorption function represents a crucial approach for preventing and treating osteoporosis. The purpose of this study was to examine the effects and molecular mechanisms of Butylphthalide (NBP) on the differentiation and function of osteoclasts induced by RANKL. Osteoclastogenesis was assessed through TRAP staining and bone slice assay. An animal model that underwent ovariectomy, simulating postmenopausal women’s physiological characteristics, was established to investigate the impact of Butylphthalide on ovariectomy-induced bone loss. To delve deeper into the specific mechanisms, we employed Western blot, PCR, immunofluorescence, and immunohistochemical staining to detect the expression of proteins that are associated with the osteoclast signaling pathway. In this study, we found that Butylphthalide not only suppressed osteoclastogenesis and bone resorption in vitro but also significantly decreased TRAcP-positive osteoclasts and prevented bone loss in vivo. Further mechanistic experiments revealed that Butylphthalide reduces intracellular ROS in osteoclasts, inhibits the MAPK and NFATc1 signaling pathways, and downregulates the key genes and proteins of osteoclasts. This inhibits osteoclast formation and function. The reduction in ROS in osteoclasts is intricately linked to the activity of Butylphthalide-modulated antioxidant enzymes. Overall, NBP may offer a alternative treatment option with fewer side effects for skeletal diseases such as osteoporosis.

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