Artykuły w czasopismach: „Osteoclastogenesis”

1

Kitaura, Hideki, Keisuke Kimura, Masahiko Ishida, Haruka Kohara, Masako Yoshimatsu i Teruko Takano-Yamamoto. "Immunological Reaction in TNF-α-Mediated Osteoclast Formation and Bone ResorptionIn VitroandIn Vivo". Clinical and Developmental Immunology 2013 (2013): 1–8. http://dx.doi.org/10.1155/2013/181849.

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Tumor necrosis factor-α(TNF-α) is a cytokine produced by monocytes, macrophages, and T cells and is induced by pathogens, endotoxins, or related substances. TNF-αmay play a key role in bone metabolism and is important in inflammatory bone diseases such as rheumatoid arthritis. Cells directly involved in osteoclastogenesis include macrophages, which are osteoclast precursor cells, osteoblasts, or stromal cells. These cells express receptor activator of NF-κB ligand (RANKL) to induce osteoclastogenesis, and T cells, which secrete RANKL, promote osteoclastogenesis during inflammation. Elucidating the detailed effects of TNF-αon bone metabolism may enable the identification of therapeutic targets that can efficiently suppress bone destruction in inflammatory bone diseases. TNF-αis considered to act by directly increasing RANK expression in macrophages and by increasing RANKL in stromal cells. Inflammatory cytokines such as interleukin- (IL-) 12, IL-18, and interferon-γ(IFN-γ) strongly inhibit osteoclast formation. IL-12, IL-18, and IFN-γinduce apoptosis in bone marrow cells treated with TNF-α in vitro, and osteoclastogenesis is inhibited by the interactions of TNF-α-induced Fas and Fas ligand induced by IL-12, IL-18, and IFN-γ. This review describes and discusses the role of cells concerned with osteoclast formation and immunological reactions in TNF-α-mediated osteoclastogenesisin vitroandin vivo.

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Fukawa, Yuki, Kou Kayamori, Maiko Tsuchiya i Tohru Ikeda. "IL-1 Generated by Oral Squamous Cell Carcinoma Stimulates Tumor-Induced and RANKL-Induced Osteoclastogenesis: A Possible Mechanism of Bone Resorption Induced by the Infiltration of Oral Squamous Cell Carcinoma". International Journal of Molecular Sciences 24, nr 1 (30.12.2022): 688. http://dx.doi.org/10.3390/ijms24010688.

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We previously observed a novel osteoclastogenesis system that is induced by oral squamous cell carcinoma (OSCC) cells, which target osteoclast precursor cells (OPC) without upregulation of the master transcriptional factor of osteoclastogenesis, NFATc1. Here, we analyzed inflammatory cytokines that were preferentially expressed in one of the osteoclastogenic OSCC cell lines, namely NEM, compared with the subclone that had lost its osteoclastogenic properties. Based on a gene expression microarray and a protein array analyses, IL-1, IL-6, IL-8, and CXCL1 were chosen as candidates responsible for tumor-induced osteoclastogenesis. From the results of the in vitro osteoclastogenesis assay using OPCs cultured with OSCC cells or their culture supernatants, IL-1 was selected as a stimulator of both OSCC-induced and RANKL-induced osteoclastogenesis. The IL-1 receptor antagonist significantly attenuated osteoclastogenesis induced by NEM cells. The stimulatory effects of IL-1 for OSCC-induced and RANKL-induced osteoclastogenesis were effectively attenuated with cannabidiol and denosumab, respectively. These results suggest that IL-1 secreted from OSCC cells stimulates not only tumor-induced osteoclastogenesis targeting OPCs but also physiological RANKL-induced osteoclastogenesis, and this may be the biological mechanism of bone resorption induced by the infiltration of OSCC. These results also suggest that IL-1 inhibitors are candidates for therapeutic agents against bone resorption induced by OSCC.

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Kim, Jung-Eun. "Osteoclastogenesis and Osteogenesis". International Journal of Molecular Sciences 23, nr 12 (15.06.2022): 6659. http://dx.doi.org/10.3390/ijms23126659.

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Legg, Katrin. "Osteoclastogenesis inhibitor identified". Nature Reviews Rheumatology 5, nr 8 (sierpień 2009): 413. http://dx.doi.org/10.1038/nrrheum.2009.128.

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Lu, Weiguang, Liu Yang i Zhuojing Luo. "Myricitrin inhibits osteoclastogenesis". Journal of Orthopaedic Translation 7 (październik 2016): 95–96. http://dx.doi.org/10.1016/j.jot.2016.06.087.

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Maruotti, Nicola, Maria Grano, Silvia Colucci, Francesca d’Onofrio i Francesco Paolo Cantatore. "Osteoclastogenesis and arthritis". Clinical and Experimental Medicine 11, nr 3 (11.11.2010): 137–45. http://dx.doi.org/10.1007/s10238-010-0117-2.

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7

Feng, Wei. "Osteoclastogenesis and osteoimmunology". Frontiers in Bioscience 19, nr 5 (2014): 758. http://dx.doi.org/10.2741/4242.

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Dou, Ce, Nan Li, Ning Ding, Chuan Liu, Xiaochao Yang, Fei Kang, Zhen Cao i in. "HDAC2 regulates FoxO1 during RANKL-induced osteoclastogenesis". American Journal of Physiology-Cell Physiology 310, nr 10 (15.05.2016): C780—C787. http://dx.doi.org/10.1152/ajpcell.00351.2015.

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The bone-resorbing osteoclast (OC) is essential for bone homeostasis, yet deregulation of OCs contributes to diseases such as osteoporosis, osteopetrosis, and rheumatoid arthritis. Here we show that histone deacetylase 2 (HDAC2) is a key positive regulator during receptor activator of nuclear factor-κB ligand (RANKL)-induced osteoclastogenesis and bone resorption. Bone marrow macrophages (BMMs) showed increased HDAC2 expression during osteoclastogenesis. HDAC2 overexpression enhanced, whereas HDAC2 deletion suppressed osteoclastogenesis and bone resorption using lentivirus infection. Mechanistically, upon RANKL activation, HDAC2 activated Akt; Akt directly phosphorylates and abrogates Forkhead box protein O1 (FoxO1), which is a negative regulator during osteoclastogenesis through reducing reactive oxygen species. HDAC2 deletion in BMMs resulted in decreased Akt activation and increased FoxO1 activity during osteoclastogenesis. In conclusion, HDAC2 activates Akt thus suppresses FoxO1 transcription results in enhanced osteoclastogenesis. Our data imply the potential value of HDAC2 as a new target in regulating osteoclast differentiation and function.

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Panahipour, Layla, Zahra Kargarpour, Maria Laggner, Michael Mildner, Hendrik J. Ankersmit i Reinhard Gruber. "TGF-β in the Secretome of Irradiated Peripheral Blood Mononuclear Cells Supports In Vitro Osteoclastogenesis". International Journal of Molecular Sciences 21, nr 22 (13.11.2020): 8569. http://dx.doi.org/10.3390/ijms21228569.

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Osteoclastogenesis required for bone remodeling is also a key pathologic mechanism of inflammatory osteolysis being controlled by paracrine factors released from dying cells. The secretome of irradiated, dying peripheral blood mononuclear cells (PBMCs) has a major impact on the differentiation of myeloid cells into dendritic cells, and macrophage polarization. The impact on osteoclastogenesis, however, has not been reported. For this aim, we used murine bone marrow macrophages exposed to RANKL and M-CSF to initiate osteoclastogenesis, with and without the secretome obtained from γ-irradiated PBMCs. We reported that the secretome significantly enhanced in vitro osteoclastogenesis as determined by means of histochemical staining of the tartrate-resistant acid phosphatase (TRAP), as well as the expression of the respective target genes, including TRAP and cathepsin K. Considering that TGF-β enhanced osteoclastogenesis, we confirmed the TGF-β activity in the secretome with a bioassay that was based on the increased expression of IL11 in fibroblasts. Neutralizing TGF-β by an antibody decreased the ability of the secretome to support osteoclastogenesis. These findings suggested that TGF-β released by irradiated PBMCs could enhance the process of osteoclastogenesis in vitro.

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Huang, Deqiu, Fujian Zhao, Wendong Gao, Xiaofeng Chen, Zhouyi Guo i Wen Zhang. "Strontium-substituted sub-micron bioactive glasses inhibit ostoclastogenesis through suppression of RANKL-induced signaling pathway". Regenerative Biomaterials 7, nr 3 (30.03.2020): 303–11. http://dx.doi.org/10.1093/rb/rbaa004.

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Abstract Strontium-substituted bioactive glass (Sr-BG) has shown superior performance in bone regeneration. Sr-BG-induced osteogenesis has been extensively studied; however, Sr-BG-mediated osteoclastogenesis and the underlying molecular mechanism remain unclear. It is recognized that the balance of osteogenesis and osteoclastogenesis is closely related to bone repair, and the receptor activators of nuclear factor kappaB ligand (RANKL) signaling pathway plays a key role of in the regulation of osteoclastogenesis. Herein, we studied the potential impact and underling mechanism of strontium-substituted sub-micron bioactive glass (Sr-SBG) on RANKL-induced osteoclast activation and differentiation in vitro. As expected, Sr-SBG inhibited RANKL-mediated osteoclastogenesis significantly with the experimental performance of decreased mature osteoclasts formation and downregulation of osteoclastogenesis-related gene expression. Furthermore, it was found that Sr-SBG might suppress osteoclastogenesis by the combined effect of strontium and silicon released through inhibition of RANKL-induced activation of p38 and NF-κB pathway. These results elaborated the effect of Sr-SBG-based materials on osteoclastogenesis through RANKL-induced downstream pathway and might represent a significant guidance for designing better bone repair materials.

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11

Yao, Chao Hua, Pei Zhang i Liang Zhang. "Differential protein and mRNA expression of CaMKs during osteoclastogenesis and its functional implications". Biochemistry and Cell Biology 90, nr 4 (sierpień 2012): 532–39. http://dx.doi.org/10.1139/o2012-002.

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The calmodulin-dependent kinase (CaMK) family has been recently recognized to participate in the regulation of osteoclastogenesis. However, there are some controversial reports regarding the mRNA expression patterns of CaMKs during osteoclastogenesis, although the protein expression pattern of most CaMKs during osteoclastogenesis have not been studied. In the present study, we attempted to address this issue by using a mouse bone marrow monocyte model and parallel Western blotting and quantitative real-time PCR. Our results revealed some interesting expression patterns of CaMKs during the process. Among all CaMKs examined, only CaMKIIδ exhibited consistent expression patterns between its mRNA and protein with both rising remarkably during osteoclastogenesis. CaMKIV protein was not detectable during the first three days of cell culture, but it rose on Day 5. The CaMK inhibitor, KN93, subdued osteoclastogenesis during the first three days of cell culture, a time when CaMKIV was absent while other KN93-sensitive CaMKs presented. In addition, KN93 was found to inhibit the expression of some early receptor activator of NF-κB (RANK) signaling intermediates (extracellular signal-regulated kinase (ERK) and Akt) in the non-differentiated mouse bone marrow monocytes. Collectively, these data reveal differential expression patterns of KN93-sensitive CaMK proteins and their mRNAs during osteoclastogenesis, supporting a CaMKII–RANK signaling interaction in the regulation of early osteoclastogenesis.

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Kamiya, Yosuke, Takeshi Kikuchi, Hisashi Goto, Iichiro Okabe, Yuhei Takayanagi, Yuki Suzuki, Noritaka Sawada i in. "IL-35 and RANKL Synergistically Induce Osteoclastogenesis in RAW264 Mouse Monocytic Cells". International Journal of Molecular Sciences 21, nr 6 (18.03.2020): 2069. http://dx.doi.org/10.3390/ijms21062069.

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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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Yamaguchi, Tsuguno, Alexandru Movila, Shinsuke Kataoka, Wichaya Wisitrasameewong, Montserrat Ruiz Torruella, Michiaki Murakoshi, Shinya Murakami i Toshihisa Kawai. "Proinflammatory M1 Macrophages Inhibit RANKL-Induced Osteoclastogenesis". Infection and Immunity 84, nr 10 (25.07.2016): 2802–12. http://dx.doi.org/10.1128/iai.00461-16.

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In response to a defined panel of stimuli, immature macrophages can be classified into two major phenotypes: proinflammatory (M1) and anti-inflammatory (M2). Although both phenotypes have been implicated in several chronic inflammatory diseases, their direct role in bone resorption remains unclear. The present study investigated the possible effects of M1 and M2 macrophages on RANKL-induced osteoclastogenesis. In osteoclastogenesis assays using RAW264.7 cells or bone marrow cells as osteoclast precursors, addition of M1 macrophages significantly suppressed RANKL-induced osteoclastogenesis compared to nonstimulated conditions (M0), addition of M2 macrophages, or no macrophage addition (P< 0.05), suggesting that M1 macrophages can downregulate osteoclastogenesis. This effect was maintained when direct contact between M1 and osteoclast precursors was interrupted by cell culture insertion, indicating engagement of soluble factors released from M1. M1 macrophages developed from interferon gamma (IFN-γ) knockout (IFN-γ–KO) mice lost the ability to downregulate osteoclastogenesis. Antibody-based neutralization of interleukin-12 (IL-12), but not IL-10, produced by M1 macrophages also abrogated M1-mediated downregulation of osteoclastogenesis. Real-time PCR analyses showed that IFN-γ suppressed gene expression of NFATc1, a master regulator of osteoclastogenesis, whereas IL-12 increased the apoptosis of osteoclasts, suggesting molecular mechanisms underlying the possible roles of IFN-γ or IL-12 in M1-mediated inhibition of osteoclastogenesis. These findings were confirmed in anin vivoligature-induced mouse periodontitis model in which adoptive transfer of M1 macrophages showed a significantly lower level of bone loss and less tartrate-resistant acid phosphatase (TRAP)-positive cell induction than M0 or M2 macrophage transfer. In conclusion, by its secretion of IFN-γ and IL-12, M1, but not M0 or M2, was demonstrated to inhibit osteoclastogenesis.

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Inubushi, T., A. Kawazoe, M. Miyauchi, S. Yanagisawa, A. Subarnbhesaj, C. Chanbora, N. F. Ayuningtyas, A. Ishikado, E. Tanaka i T. Takata. "Lactoferrin inhibits infection-related osteoclastogenesis without interrupting compressive force-related osteoclastogenesis". Archives of Oral Biology 59, nr 2 (luty 2014): 226–32. http://dx.doi.org/10.1016/j.archoralbio.2013.11.002.

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Miyauchi, Yoshiteru, Ken Ninomiya, Hiroya Miyamoto, Akemi Sakamoto, Ryotaro Iwasaki, Hiroko Hoshi, Kana Miyamoto i in. "The Blimp1–Bcl6 axis is critical to regulate osteoclast differentiation and bone homeostasis". Journal of Experimental Medicine 207, nr 4 (5.04.2010): 751–62. http://dx.doi.org/10.1084/jem.20091957.

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Controlling osteoclastogenesis is critical to maintain physiological bone homeostasis and prevent skeletal disorders. Although signaling activating nuclear factor of activated T cells 1 (NFATc1), a transcription factor essential for osteoclastogenesis, has been intensively investigated, factors antagonistic to NFATc1 in osteoclasts have not been characterized. Here, we describe a novel pathway that maintains bone homeostasis via two transcriptional repressors, B cell lymphoma 6 (Bcl6) and B lymphocyte–induced maturation protein-1 (Blimp1). We show that Bcl6 directly targets ‘osteoclastic’ molecules such as NFATc1, cathepsin K, and dendritic cell-specific transmembrane protein (DC-STAMP), all of which are targets of NFATc1. Bcl6-overexpression inhibited osteoclastogenesis in vitro, whereas Bcl6-deficient mice showed accelerated osteoclast differentiation and severe osteoporosis. We report that Bcl6 is a direct target of Blimp1 and that mice lacking Blimp1 in osteoclasts exhibit osteopetrosis caused by impaired osteoclastogenesis resulting from Bcl6 up-regulation. Indeed, mice doubly mutant in Blimp1 and Bcl6 in osteoclasts exhibited decreased bone mass with increased osteoclastogenesis relative to osteoclast-specific Blimp1-deficient mice. These results reveal a Blimp1–Bcl6–osteoclastic molecule axis, which critically regulates bone homeostasis by controlling osteoclastogenesis and may provide a molecular basis for novel therapeutic strategies.

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Lee, Youngkyun, Seok-Won Hyung, Hee Jung Jung, Hyung-Joon Kim, Judith Staerk, Stefan N. Constantinescu, Eun-Ju Chang, Zang Hee Lee, Sang-Won Lee i Hong-Hee Kim. "The ubiquitin-mediated degradation of Jak1 modulates osteoclastogenesis by limiting interferon-β–induced inhibitory signaling". Blood 111, nr 2 (15.01.2008): 885–93. http://dx.doi.org/10.1182/blood-2007-03-082941.

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Interferons (IFNs) have been shown to negatively regulate osteoclastogenesis. In a proteomic study to assess protein expression during osteoclastogenesis, we discovered that the expression level of Jak1 was significantly decreased during the early stage of osteoclast differentiation from mouse bone marrow macrophages (BMMs) upon stimulation with receptor activator of nuclear factor κB ligand (RANKL). RANKL induced Jak1 ubiquitination, and a proteasome inhibitor MG132 efficiently blocked the RANKL-induced degradation of Jak1. The expression level of Jak1 correlated with the susceptibility of osteoclast precursors to the negative regulatory effects of IFN-β on osteoclastogenesis, since preosteoclasts (pOCs) in which Jak1 expression is significantly reduced could proceed with osteoclastogenesis in the presence of IFN-β. Forced down-regulation of Jak1 by small interfering RNA (siRNA) resulted in the efficient osteoclast differentiation of BMMs in the presence of inhibitory IFN-β, while overexpression of Jak1 in pOCs elicited IFN-β–dependent inhibition of osteoclastogenesis. Furthermore, we found that the IFN-β–induced inhibition of osteoclastogenesis required STAT3 downstream of Jak1. These data suggest that the regulation of Jak1 expression during osteoclast differentiation might serve as an intrinsic mechanism that determines osteoclast lineage commitment by modulating the negative regulation by IFN-β.

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Ding, Mina, Zhihao Chen, Eunjin Cho, Sang-Wook Park i Tae-Hoon Lee. "Crucial Role of Lysine-Specific Histone Demethylase 1 in RANKL-Mediated Osteoclast Differentiation". International Journal of Molecular Sciences 24, nr 4 (10.02.2023): 3605. http://dx.doi.org/10.3390/ijms24043605.

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Epigenetic regulators are involved in osteoclast differentiation. This study proposes that the inhibitors of epigenetic regulators could be effective in the treatment of osteoporosis. This study identified GSK2879552, a lysine-specific histone demethylase 1 (LSD1) inhibitor, as a candidate for the treatment of osteoporosis from epigenetic modulator inhibitors. We investigate the function of LSD1 during RANKL-induced osteoclast formation. LSD1 small-molecule inhibitors effectively inhibit the RANKL-induced osteoclast differentiation in a dose-dependent manner. LSD1 gene knockout in macrophage cell line Raw 264.7 also inhibits RANKL-mediated osteoclastogenesis. LSD1-inhibitor-treated primary macrophage cells and LSD1 gene knockout Raw 264.7 cells failed to show actin ring formation. LSD1 inhibitors prevent the expression of RANKL-induced osteoclast-specific genes. They also downregulated the protein expression of osteoclast-related markers in osteoclastogeneses, such as Cathepsin K, c-Src, and NFATc1. Although LSD1 inhibitors were shown to reduce the in vitro demethylation activity of LSD1, they did not modulate the methylation of Histone 3 K4 and K9 during osteoclastogenesis. The ovariectomy (OVX)-induced osteoporosis model revealed that GSK2879552 slightly restores OVX-induced cortical bone loss. LSD1 can be employed as a positive regulator to promote osteoclast formation. Hence, inhibition of LSD1 activities is a potential target for preventing bone diseases characterized by excessive osteoclast activities.

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Kang, J. H., H. M. Ko, J. S. Moon, H. I. Yoo, J. Y. Jung, M. S. Kim, J. T. Koh, W. J. Kim i S. H. Kim. "Osteoprotegerin Expressed by Osteoclasts". Journal of Dental Research 93, nr 11 (25.09.2014): 1116–23. http://dx.doi.org/10.1177/0022034514552677.

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Osteoprotegerin (OPG) is secreted by stromal and osteoblastic lineage cells and inhibits osteoclastogenesis by preventing the interaction of receptor activator of nuclear factor-κB ligand (RANKL) with receptor activator of nuclear factor-κB (RANK). In this study, the expression of OPG in osteoclasts themselves and its biological functions during osteoclastogenesis were investigated for the first time. OPG expression in vivo in the developing rat maxilla was examined by immunofluorescence analysis. OPG expression in osteoclasts during in vitro osteoclastogenesis was determined by reverse-transcription polymerase chain-reaction (RT-PCR), Western blot, and immunofluorescence staining. We determined the function of OPG produced by osteoclasts during osteoclastogenesis by silencing the OPG gene. The effects of OPG on bone-resorbing activity and apoptosis of mature osteoclasts were examined by the assay of resorptive pit formation on calcium-phosphate-coated plate and terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL) staining, respectively. In the immunofluorescence findings, strong immunoreactivities were unexpectedly seen in multinucleated tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts around the growing and erupting tooth germs in the rat alveolar bone. In vitro, OPG expression was significantly increased during the differentiation of osteoclasts from mouse bone-marrow-derived cells treated with a combination of macrophage colony-stimulating factor (M-CSF) and RANKL. Interestingly, it was found that OPG small interfering (si)RNA treatment during osteoclastogenesis enhanced the sizes of osteoclasts, but attenuated their bone-resorbing activity. Also, the increased chromosomal DNA fragmentation and caspase-3 activity in the late phase of osteoclastogenesis were found to be decreased by treatment with OPG siRNA. Furthermore, effects of OPG siRNA treatment on osteoclastogenesis and bone-resorbing activity were recovered by the treatment of exogenous OPG. These results suggest that OPG, expressed by the osteoclasts themselves, may play an auto-regulatory role in the late phase of osteoclastogenesis through the induction of apoptosis.

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Kitaura, H., M. Yoshimatsu, Y. Fujimura, T. Eguchi, H. Kohara, A. Yamaguchi i N. Yoshida. "An Anti-c-Fms Antibody Inhibits Orthodontic Tooth Movement". Journal of Dental Research 87, nr 4 (kwiecień 2008): 396–400. http://dx.doi.org/10.1177/154405910808700405.

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Orthodontic force induces osteoclastogenesis in vivo. It has recently been reported that administration of an antibody against the macrophage-colony-stimulating factor (M-CSF) receptor c-Fms blocks osteoclastogenesis and bone erosion induced by tumor necrosis factor-α (TNF-α) administration. This study aimed to examine the effect of an anti-c-Fms antibody on mechanical loading-induced osteoclastogenesis and osteolysis in an orthodontic tooth movement model in mice. Using TNF receptor 1- and 2-deficient mice, we showed that orthodontic tooth movement was mediated by TNF-α. We injected anti-c-Fms antibody daily into a local site, for 12 days, during mechanical loading. The anti-c-Fms antibody significantly inhibited orthodontic tooth movement, markedly reduced the number of osteoclasts in vivo, and inhibited TNF-α-induced osteoclastogenesis in vitro. These findings suggest that M-CSF plays an important role in mechanical loading-induced osteoclastogenesis and bone resorption during orthodontic tooth movement mediated by TNF-α.

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Liu, Jie, Jun Shiono, Yukiko Tsuji, Kuniyoshi Shimizu i Ryuichiro Kondo. "Methyl Ganoderic Acid DM: A Selective Potent Osteoclastogenesis Inhibitor". Open Bioactive Compounds Journal 2, nr 1 (26.11.2009): 37–42. http://dx.doi.org/10.2174/1874847300902010037.

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Increased osteoclastic bone resorption plays a central role in the pathogenesis of many bone diseases, and osteoclast inhibitors are the most widely used treatments for these diseases. Ganoderic acid DM, the main component of Ganoderma lucidum, has been known for its medicinal effects such as anti-androgen and anti-proliferative activities. In this study, we investigated the inhibitory effects of ganoderic acid DM and its analog (methyl ganoderic acid DM and 7-oxo-methyl ganoderic acid Z) on osteoclastogenesis using RAW264 cell in vitro. Methyl ganoderic acid DM blocked osteoclastogenesis completely at 12.5 μM with low cytotoxicity less than 30%. On the other hands, ganoderic acid DM blocked osteoclastogenesis completely at the higher concentration of 50 μM, but 7-oxo-methyl ganoderic acid Z did not up to 100 μM. These results implicated the carbonyl group at C-3 is essentially for selective osteoclastogenesis inhibitory activity, and methyl esters at C-26 should play an important role in enhancing its osteoclastogenesis inhibitory activity

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Tong, Xishuai, Gengsheng Yu, Xiaohui Fu, Ruilong Song, Jianhong Gu i Zongping Liu. "A Review of Signaling Transduction Mechanisms in Osteoclastogenesis Regulation by Autophagy, Inflammation, and Immunity". International Journal of Molecular Sciences 23, nr 17 (30.08.2022): 9846. http://dx.doi.org/10.3390/ijms23179846.

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Osteoclastogenesis is an ongoing rigorous course that includes osteoclast precursors fusion and bone resorption executed by degradative enzymes. Osteoclastogenesis is controlled by endogenous signaling and/or regulators or affected by exogenous conditions and can also be controlled both internally and externally. More evidence indicates that autophagy, inflammation, and immunity are closely related to osteoclastogenesis and involve multiple intracellular organelles (e.g., lysosomes and autophagosomes) and certain inflammatory or immunological factors. Based on the literature on osteoclastogenesis induced by different regulatory aspects, emerging basic cross-studies have reported the emerging disquisitive orientation for osteoclast differentiation and function. In this review, we summarize the partial potential therapeutic targets for osteoclast differentiation and function, including the signaling pathways and various cellular processes.

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Heo, Soon Chul, Yu Na Kim, YunJeong Choi, Ji-Young Joo, Jae Joon Hwang, Moon-Kyoung Bae i Hyung Joon Kim. "Elevated Expression of Cathepsin K in Periodontal Ligament Fibroblast by Inflammatory Cytokines Accelerates Osteoclastogenesis via Paracrine Mechanism in Periodontal Disease". International Journal of Molecular Sciences 22, nr 2 (12.01.2021): 695. http://dx.doi.org/10.3390/ijms22020695.

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Cathepsin K (CTSK) is a cysteine protease that is mainly produced from mature osteoclasts and contributes to the destruction of connective tissues and mineralized matrix as a consequence of periodontal disease (PD). However, few studies have reported its regulatory role in osteoclastogenesis-supporting cells in inflammatory conditions. Here, we investigated the role of CTSK in osteoclastogenesis-supporting cells, focusing on the modulation of paracrine function. Microarray data showed that CTSK was upregulated in PD patients compared with healthy individuals, which was further supported by immunohistochemistry and qPCR analyses performed with human gingival tissues. The expression of CTSK in the osteoclastogenesis-supporting cells, including dental pulp stem cells, gingival fibroblasts, and periodontal ligament fibroblasts (PDLFs) was significantly elevated by treatment with inflammatory cytokines such as TNFα and IL-1β. Moreover, TNFα stimulation potentiated the PDLF-mediated osteoclastogenesis of bone marrow-derived macrophages. Interestingly, small interfering RNA-mediated silencing of CTSK in PDLF noticeably attenuated the TNFα-triggered upregulation of receptor activator of nuclear factor kappa-B ligand (RANKL), macrophage colony-stimulating factor, and RANKL/osteoprotegerin ratio, thereby abrogating the enhanced osteoclastogenesis-supporting activity of PDLF. Collectively, these results suggest a novel role of CTSK in the paracrine function of osteoclastogenesis-supporting cells in periodontal disease.

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Ashtar, Mohannad, Hirofumi Tenshin, Jumpei Teramachi, Ariunzaya Bat-Erdene, Masahiro Hiasa, Asuka Oda, Kotaro Tanimoto i in. "The Roles of ROS Generation in RANKL-Induced Osteoclastogenesis: Suppressive Effects of Febuxostat". Cancers 12, nr 4 (9.04.2020): 929. http://dx.doi.org/10.3390/cancers12040929.

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Receptor activator of NF-κB ligand (RANKL), a critical mediator of osteoclastogenesis, is upregulated in multiple myeloma (MM). The xanthine oxidase inhibitor febuxostat, clinically used for prevention of tumor lysis syndrome, has been demonstrated to effectively inhibit not only the generation of uric acid but also the formation of reactive oxygen species (ROS). ROS has been demonstrated to mediate RANKL-mediated osteoclastogenesis. In the present study, we therefore explored the role of cancer-treatment-induced ROS in RANKL-mediated osteoclastogenesis and the suppressive effects of febuxostat on ROS generation and osteoclastogenesis. RANKL dose-dependently induced ROS production in RAW264.7 preosteoclastic cells; however, febuxostat inhibited the RANKL-induced ROS production and osteoclast (OC) formation. Interestingly, doxorubicin (Dox) further enhanced RANKL-induced osteoclastogenesis through upregulation of ROS production, which was mostly abolished by addition of febuxostat. Febuxostat also inhibited osteoclastogenesis enhanced in cocultures of bone marrow cells with MM cells. Importantly, febuxostat rather suppressed MM cell viability and did not compromise Dox’s anti-MM activity. In addition, febuxostat was able to alleviate pathological osteoclastic activity and bone loss in ovariectomized mice. Collectively, these results suggest that excessive ROS production by aberrant RANKL overexpression and/or anticancer treatment disadvantageously impacts bone, and that febuxostat can prevent the ROS-mediated osteoclastic bone damage.

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Sugatani, Toshifumi, Jean Vacher i Keith A. Hruska. "A microRNA expression signature of osteoclastogenesis". Blood 117, nr 13 (31.03.2011): 3648–57. http://dx.doi.org/10.1182/blood-2010-10-311415.

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Abstract MicroRNAs (miRs) are small noncoding RNAs that principally function in the spatiotemporal regulation of protein translation in animal cells. Although emerging evidence suggests that some miRs play important roles in osteoblastogenesis and skeletal homeostasis, much less is known in osteoclastogenesis. Here, we show that receptor activator of nuclear factor κB ligand (RANKL)–induced osteoclastogenesis is mediated by miR-21. MiR-21 was identified as an miR expression signature of RANKL-induced osteoclastogenesis that down-regulates programmed cell death 4 (PDCD4) protein levels. Diminished PDCD4 removes a repression from c-Fos, a critical transcription factor for osteoclastogenesis and osteoclast-specific downstream target genes. In addition, RANKL-induced c-Fos up-regulates miR-21 gene expression. Bone marrow–derived monocyte/macrophage precursors deficient of DiGeorge syndrome critical region gene 8, an RNA binding protein associated with miR biogenesis, and Dicer, an endoribonuclease in the RNaseIII family associated with miR biogenesis, possessed significantly decreased miR-21 levels and increased PDCD4 protein levels so that RANKL-induced osteoclastogenesis was impaired in those cells. However, forced expression of miR-21 rescued osteoclast development because of down-regulation of PDCD4 protein expression levels. Thus, our studies provide a new molecular mechanism, including a positive feedback loop of c-Fos/miR-21/PDCD4, regulating osteoclastogenesis.

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Tsuchiya, Maiko, Kou Kayamori, Akane Wada, Motohiro Komaki, Yae Ohata, Miwako Hamagaki, Kei Sakamoto i Tohru Ikeda. "A Novel, Tumor-Induced Osteoclastogenesis Pathway Insensitive to Denosumab but Interfered by Cannabidiol". International Journal of Molecular Sciences 20, nr 24 (9.12.2019): 6211. http://dx.doi.org/10.3390/ijms20246211.

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Bone metabolism is strictly regulated, and impaired regulation caused by hormonal imbalances induces systemic bone loss. Local bone loss caused by tumor invasion into bone is suggested to be induced by the generation of cytokines, which affect bone metabolism, by tumor cells. The major cause of systemic and local bone losses is excess bone resorption by osteoclasts, which differentiate from macrophages by receptor activator of nuclear factor kappa-B ligand (RANKL) or tumor necrosis factor-alpha (TNF-α). We previously found a novel pathway for tumor-induced osteoclastogenesis targeting osteoclast precursor cells (OPCs). Tumor-induced osteoclastogenesis was resistant to RANKL and TNF-α inhibitors. In the present study, we confirmed that exosomes derived from oral squamous cell carcinoma (OSCC) cells induced osteoclasts from OPCs. We also showed that the depletion of exosomes from culture supernatants of OSCC cells partially interfered with osteoclastogenesis, and cannabidiol, an innoxious cannabinoid without psychotropic effects, almost completely suppressed tumor-induced osteoclastogenesis. Osteoclastogenesis and its interference by cannabidiol were independent of the expression of nuclear factor of T cell c1 (NFATc1). These results show that osteoclastogenesis induced by OSCC cells targeting OPCs is a novel osteoclastogenic pathway independent of NFATc1 expression that is partially caused by tumor-derived exosomes and suppressed by cannabidiol.

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26

Fujimura, Yuji, Hitoshi Hotokezaka, Naoya Ohara, Mariko Naito, Eiko Sakai, Mamiko Yoshimura, Yuka Narita, Hideki Kitaura, Noriaki Yoshida i Koji Nakayama. "The Hemoglobin Receptor Protein of Porphyromonas gingivalis Inhibits Receptor Activator NF-κB Ligand-Induced Osteoclastogenesis from Bone Marrow Macrophages". Infection and Immunity 74, nr 5 (maj 2006): 2544–51. http://dx.doi.org/10.1128/iai.74.5.2544-2551.2006.

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ABSTRACT Extracellular proteinaceous factors of Porphyromonas gingivalis, a periodontal pathogen, that influence receptor activator of nuclear factor-κB (NF-κB) ligand (RANKL)-induced osteoclastogenesis from bone marrow macrophages were investigated. The culture supernatant of P. gingivalis had the ability to inhibit RANKL-induced in vitro osteoclastogenesis. A major protein of the culture supernatant, hemoglobin receptor protein (HbR), suppressed RANKL-induced osteoclastogenesis in a dose-dependent fashion. HbR markedly inhibited RANKL-induced osteoclastogenesis when present in the culture for the first 24 h after addition of RANKL, whereas no significant inhibition was observed when HbR was added after 24 h or later, implying that HbR might interfere with only the initial stage of RANKL-mediated differentiation. HbR tightly bound to bone marrow macrophages and had the ability to induce phosphorylation of ERK, p38, NF-κB, and Akt. RANKL-induced phosphorylation of ERK, p38, and NF-κB was not suppressed by HbR, but that of Akt was markedly suppressed. HbR inhibited RANKL-mediated induction of c-Fos and NFATc1. HbR could induce beta interferon (IFN-β) from bone marrow macrophages, but the induction level of IFN-β might not be sufficient to suppress RANKL-mediated osteoclastogenesis, implying presence of an IFN-β-independent pathway in HbR-mediated inhibition of osteoclastogenesis. Since rapid and extensive destruction of the alveolar bone causes tooth loss, resulting in loss of the gingival crevice that is an anatomical niche for periodontal pathogens such as P. gingivalis, the suppressive effect of HbR on osteoclastogenesis may help the microorganism exist long in the niche.

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Lu, Ssu-Yi, Mengtao Li i Yi-Ling Lin. "Mitf Induction by RANKL Is Critical for Osteoclastogenesis". Molecular Biology of the Cell 21, nr 10 (15.05.2010): 1763–71. http://dx.doi.org/10.1091/mbc.e09-07-0584.

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Microphthalmia-associated transcription factor (Mitf) regulates the development and function of several cell lineages, including osteoclasts. In this report, we identified a novel mechanism by which RANKL regulates osteoclastogenesis via induction of Mitf isoform E (Mitf-E). Both Mitf-A and Mitf-E are abundantly present in osteoclasts. Unlike Mitf-A, which is ubiquitously expressed and is present in similar amounts in macrophages and osteoclasts, Mitf-E is almost nondetectable in macrophages, but its expression is significantly up-regulated during osteoclastogenesis. In addition to their different expression profiles, the two isoforms are drastically different in their abilities to support osteoclastogenesis, despite sharing all known functional domains. Unlike Mitf-A, small amounts of Mitf-E are present in nuclear lysates unless chromatin is digested/sheared during the extraction. Based on these data, we propose a model in which Mitf-E is induced during osteoclastogenesis and is closely associated with chromatin to facilitate its interaction with target promoters; therefore, Mitf-E has a stronger osteoclastogenic activity. Mitf-A is a weaker osteoclastogenic factor, but activated Mitf-A alone is not sufficient to fully support osteoclastogenesis. Therefore, this receptor activator for nuclear factor-κB ligand (RANKL)-induced Mitf phenomenon seems to play an important role during osteoclastogenesis. Although the current theory indicates that Mitf and its binding partner Tfe3 are completely redundant in osteoclasts, using RNA interference, we demonstrated that Mitf has a distinct role from Tfe3. This study provides the first evidence that RANKL-induced Mitf is critical for osteoclastogenesis and Mitf is not completely redundant with Tfe3.

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28

Xu, Shuyu, i Zuolin Wang. "Bone marrow mesenchymal stem cell-derived exosomes enhance osteoclastogenesis during alveolar bone deterioration in rats". RSC Advances 7, nr 34 (2017): 21153–63. http://dx.doi.org/10.1039/c6ra27931g.

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BMMSC-derived exosomes from rats with bone deterioration increased the osteoclastogenesis of the Raw264.7 cells, which suggests that BMMSC-derived exosomes could accelerate osteoclastogenesis in alveolar bone deterioration.

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29

Mun, Se Hwan, Brian Oh, Min Joon Lee, Seyeon Bae, Young Yang i Kyung-Hyun Park-Min. "THOC5 regulates human osteoclastogenesis". European Journal of Cell Biology 101, nr 3 (sierpień 2022): 151248. http://dx.doi.org/10.1016/j.ejcb.2022.151248.

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Mun, Se Hwan, Brian Oh, Min Joon Lee, Seyeon Bae, Young Yang i Kyung-Hyun Park-Min. "THOC5 regulates human osteoclastogenesis". European Journal of Cell Biology 101, nr 3 (sierpień 2022): 151248. http://dx.doi.org/10.1016/j.ejcb.2022.151248.

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31

Smith, Katherine. "Two Notches in osteoclastogenesis". Nature Reviews Rheumatology 8, nr 5 (27.03.2012): 247. http://dx.doi.org/10.1038/nrrheum.2012.46.

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von Metzler, I., H. Krebbel, M. Hecht, R. A. Manz, C. Fleissner, M. Mieth, M. Kaiser i in. "Bortezomib inhibits human osteoclastogenesis". Leukemia 21, nr 9 (21.06.2007): 2025–34. http://dx.doi.org/10.1038/sj.leu.2404806.

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Zavrski, Ivana, Monica Hecht, Holger Krebbel, Claudia Fleissner, Maren Mieth, Martin Kaiser, Ulrike Heider i in. "Bortezomib Inhibits Human Osteoclastogenesis." Blood 108, nr 11 (16.11.2006): 1395. http://dx.doi.org/10.1182/blood.v108.11.1395.1395.

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Abstract Enhanced osteoclastogenesis in cancer-induced bone disease may be caused by intercellular interactions between tumor cells and cells of the bone marrow microenvironment. In multiple myeloma, overexpression of RANKL in the bone marrow microenvironment may lead to the activation of TRAF-signaling and in consequence to increased NF-κB and AP-1 transcriptional activities in osteoclastic lineage cells. This results in enhanced osteoclast differentiation, activation and increased bone resorption. In this study, we have examined the effects of two NF-κB inhibitors towards their inhibitory potency on human osteoclastogenesis: proteasome inhibitor bortezomib and selective IKK inhibitor PS-1145. CD14+ osteoclast precursors from peripheral blood were stimulated with RANKL and M-CSF up to four weeks. Using MTT- and TUNEL-assays, cytotoxicity levels of each drug were determined on the differentiation stage day +1 (early osteoclast precursors), day +8 (preosteoclasts) and day +21 (osteoclasts). To evaluate the effects of both drugs considering osteoclast differentiation and -function, 2 sub-apoptotic doses of bortezomib, one sub-apoptotic and one low-apoptotic dose of PS-1145 were used. As revealed by the microscopic quantification of mature osteoclasts (TRAP-positive and multi-nucleated cells), the osteoclast differentiation was diminished by both drugs, whereas the effects were dose- and time-dependent. The microscopic quantification of resorption lacunae on dentine pits revealed that the resorptional activity was reduced by 65% for 0.1 nM bortezomib (p=0.007), by 79% for 1 nM bortezomib (p<0.0005), by 60% for 1 μM PS-1145 (p=0.023) and by 91% for 10 μM PS-1145 (p<0.0005). As shown by immunoblotting and by ELISA-based methods, the subcellular mechanisms of action involved in inhibition of early osteoclast differentiation were found to be related to the inhibition of p38 mitogen-activated protein kinase (MAPK) pathways, whereas the advanced differentiation and activation occurred in course of inhibition of AP-1 and NF-κB activation. The AP-1 blockade contributed to significant reduction of osteoclastic vascular endothelial growth factor (VEGF) production. In conclusion, our data demonstrate that proteasomal inhibition should be considered as a novel therapeutical principle of cancer-induced lytic bone disease.

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O'Brien, Charles A., Tomoki Nakashima i Hiroshi Takayanagi. "Osteocyte control of osteoclastogenesis". Bone 54, nr 2 (czerwiec 2013): 258–63. http://dx.doi.org/10.1016/j.bone.2012.08.121.

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Lee, Sang-Heon. "Osteoclastogenesis in Rheumatoid Arthritis". Journal of Rheumatic Diseases 18, nr 2 (2011): 71. http://dx.doi.org/10.4078/jrd.2011.18.2.71.

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Collison, Joanna. "DJ-1 orchestrates osteoclastogenesis". Nature Reviews Rheumatology 14, nr 1 (30.11.2017): 3. http://dx.doi.org/10.1038/nrrheum.2017.199.

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Collison, Joanna. "ER stress causes osteoclastogenesis". Nature Reviews Rheumatology 14, nr 4 (15.02.2018): 184. http://dx.doi.org/10.1038/nrrheum.2018.24.

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Onuora, Sarah. "Potassium channel regulates osteoclastogenesis". Nature Reviews Rheumatology 14, nr 2 (luty 2018): 64. http://dx.doi.org/10.1038/nrrheum.2018.7.

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Luukkonen, Jani, Johanna Huhtakangas, Sanna Palosaari, Juha Tuukkanen, Olli Vuolteenaho i Petri Lehenkari. "Preliminary Report: Osteoarthritis and Rheumatoid Arthritis Synovial Fluid Increased Osteoclastogenesis In Vitro by Monocyte Differentiation Pathway Regulating Cytokines". Mediators of Inflammation 2022 (31.05.2022): 1–13. http://dx.doi.org/10.1155/2022/2606916.

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Background. Rheumatoid arthritis (RA) and osteoarthritis (OA) are common joint diseases associated with changes in local, as well as systemic bone structure and osteoclast function. We investigated how the different soluble inflammatory stimuli in these diseases can affect osteoclastogenesis and bone resorption in vitro. Methods. Human peripheral blood mononuclear cell-derived osteoclasts were cultured on bone slices with serum from treatment-naïve RA patients and healthy controls and with synovial fluid samples acquired from RA and OA patients. The concentrations of 29 different cytokines and related proteins, including RANKL and OPG, were analyzed in the fluids tested. Results. RA serum and synovial fluid increased both osteoclastogenesis and bone resorption. Osteoclastogenesis and activity increased more in the cultures containing OA than RA synovial fluid. The osteoclasts cultured in different culture media exhibited different phenotypes, especially the cells cultured with OA synovial fluid were generally larger and had more nuclei. A general increase in proinflammatory cytokines in RA synovial fluid and serum was found. Surprisingly, OA synovial fluid showed lower levels of osteoclastogenesis inhibiting cytokines, such as IL-4 and IL-10, than RA synovial fluid, which at least partly explains more pronounced osteoclastogenesis. No significant difference was found in RANKL or OPG levels. Conclusion. The proinflammatory stimulus in OA and RA drives the monocyte differentiation towards inflammatory osteoclastogenesis and altered osteoclast phenotype.

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40

Zhao, Baohong, Shannon N. Grimes, Susan Li, Xiaoyu Hu i Lionel B. Ivashkiv. "TNF-induced osteoclastogenesis and inflammatory bone resorption are inhibited by transcription factor RBP-J". Journal of Experimental Medicine 209, nr 2 (16.01.2012): 319–34. http://dx.doi.org/10.1084/jem.20111566.

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Tumor necrosis factor (TNF) plays a key role in the pathogenesis of inflammatory bone resorption and associated morbidity in diseases such as rheumatoid arthritis and periodontitis. Mechanisms that regulate the direct osteoclastogenic properties of TNF to limit pathological bone resorption in inflammatory settings are mostly unknown. Here, we show that the transcription factor recombinant recognition sequence binding protein at the Jκ site (RBP-J) strongly suppresses TNF-induced osteoclastogenesis and inflammatory bone resorption, but has minimal effects on physiological bone remodeling. Myeloid-specific deletion of RBP-J converted TNF into a potent osteoclastogenic factor that could function independently of receptor activator of NF-κB (RANK) signaling. In the absence of RBP-J, TNF effectively induced osteoclastogenesis and bone resorption in RANK-deficient mice. Activation of RBP-J selectively in osteoclast precursors suppressed inflammatory osteoclastogenesis and arthritic bone resorption. Mechanistically, RBP-J suppressed induction of the master regulator of osteoclastogenesis (nuclear factor of activated T cells, cytoplasmic 1) by attenuating c-Fos activation and suppressing induction of B lymphocyte–induced maturation protein-1, thereby preventing the down-regulation of transcriptional repressors such as IRF-8 that block osteoclast differentiation. Thus, RBP-J regulates the balance between activating and repressive signals that regulate osteoclastogenesis. These findings identify RBP-J as a key upstream negative regulator of osteoclastogenesis that restrains excessive bone resorption in inflammatory settings.

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Ohori, Fumitoshi, Hideki Kitaura, Saika Ogawa, Wei-Ren Shen, Jiawei Qi, Takahiro Noguchi, Aseel Marahleh, Yasuhiko Nara, Adya Pramusita i Itaru Mizoguchi. "IL-33 Inhibits TNF-α-Induced Osteoclastogenesis and Bone Resorption". International Journal of Molecular Sciences 21, nr 3 (8.02.2020): 1130. http://dx.doi.org/10.3390/ijms21031130.

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Interleukin (IL)-33 is a member of the IL-1 family, which acts as an alarmin. Several studies suggested that IL-33 inhibited osteoclastogenesis and bone resorption. Tumor necrosis factor-α (TNF-α) is considered a direct inducer of osteoclastogenesis. However, there has been no report regarding the effect of IL-33 on TNF-α-induced osteoclastogenesis and bone resorption. The objective of this study is to investigate the role of IL-33 on TNF-α-induced osteoclastogenesis and bone resorption. In an in vitro analysis of osteoclastogenesis, osteoclast precursors, which were derived from bone marrow cells, were treated with or without IL-33 in the presence of TNF-α. Tartrate-resistant acid phosphatase (TRAP) staining solution was used to assess osteoclast formation. In an in vivo analysis of mouse calvariae, TNF-α with or without IL-33 was subcutaneously administrated into the supracalvarial region of mice daily for 5 days. Histological sections were stained for TRAP, and osteoclast numbers were determined. Using micro-CT reconstruction images, the ratio of bone destruction area on the calvariae was evaluated. The number of TRAP-positive cells induced by TNF-α was significantly decreased with IL-33 in vitro and in vivo. Bone resorption was also reduced. IL-33 inhibited IκB phosphorylation and NF-κB nuclear translocation. These results suggest that IL-33 inhibited TNF-α-induced osteoclastogenesis and bone resorption.

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42

Duplomb, Laurence, Marc Baud’huin, Céline Charrier, Martine Berreur, Valérie Trichet, Frédéric Blanchard i Dominique Heymann. "Interleukin-6 Inhibits Receptor Activator of Nuclear Factor κB Ligand-Induced Osteoclastogenesis by Diverting Cells into the Macrophage Lineage: Key Role of Serine727 Phosphorylation of Signal Transducer and Activator of Transcription 3". Endocrinology 149, nr 7 (10.04.2008): 3688–97. http://dx.doi.org/10.1210/en.2007-1719.

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Osteoclasts are bone-resorptive cells that differentiate from hematopoietic precursors upon receptor activator of nuclear factor κB ligand (RANKL) activation. Previous studies demonstrated that IL-6 indirectly stimulates osteoclastogenesis through the production of RANKL by osteoblasts. However, few data described the direct effect of IL-6 on osteoclasts. To investigate this effect, we used several models: murine RAW264.7 cells, mouse bone marrow, and human blood monocytes. In the three models used, the addition of IL-6 inhibited RANKL-induced osteoclastogenesis. Furthermore, IL-6 decreased the expression of osteoclast markers and up-modulated macrophage markers. To elucidate this inhibition, signal transducer and activator of transcription (STAT) 3, the main signaling molecule activated by IL-6, was analyzed. Addition of two STAT3 inhibitors completely abolished RANKL-induced osteoclastogenesis, revealing a key role of STAT3. We demonstrated that a basal level of phosphorylated-STAT3 on Serine727 associated with an absence of phosphorylation on Tyrosine705 is essential for osteoclastogenesis. Furthermore, a decrease of Serine727 phosphorylation led to an inhibition of osteoclast differentiation, whereas an increase of Tyrosine705 phosphorylation upon IL-6 stimulation led to the formation of macrophages instead of osteoclasts. In conclusion, we showed for the first time that IL-6 inhibits RANKL-induced osteoclastogenesis by diverting cells into the macrophage lineage, and demonstrated the functional role of activated-STAT3 and its form of phosphorylation in the control of osteoclastogenesis.

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Arai, Satoshi, Norio Amizuka, Yoshiaki Azuma, Sunao Takeshita i Akira Kudo. "Osteoclastogenesis-Related Antigen, a Novel Molecule on Mouse Stromal Cells, Regulates Osteoclastogenesis". Journal of Bone and Mineral Research 18, nr 4 (1.04.2003): 686–95. http://dx.doi.org/10.1359/jbmr.2003.18.4.686.

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Chen, Xiao, Xiaoqun Li, Xiao Zhai, Xin Zhi, Liehu Cao, Longjuan Qin i Jiacan Su. "Shikimic Acid Inhibits Osteoclastogenesis in Vivo and in Vitro by Blocking RANK/TRAF6 Association and Suppressing NF-κB and MAPK Signaling Pathways". Cellular Physiology and Biochemistry 51, nr 6 (2018): 2858–71. http://dx.doi.org/10.1159/000496039.

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Background/Aims: Bone homeostasis is associated with the balance between bone-resorbing osteoclasts and bone-forming osteoblasts. Unbalanced bone homeostasis as a result of reduced osteogenesis or excessive osteoclastogenesis can lead to disorders such as osteoporosis, Paget’s disease, and rheumatoid arthritis. Shikimic acid is a cyclohexanecarboxylic acid, reported to exhibit pharmacological properties including anti-inflammatory and antioxidant activities. However, its effects on bone homeostasis remain unknown. Methods: First, the in vitro MTT cell viability assay was performed. Tartrate-resistant acid phosphatase (TRAP) and actin ring formation assays, as well as immunofluorescence staining were then performed to evaluate osteoclastogenesis. Potential signaling pathways were characterized by western blotting and verified in overexpression experiments. Related factors were examined by western blotting, reverse transcription polymerase chain reaction, electrophoretic mobility shift assay, and co-immunoprecipitation. Ovariectomized mice were used for the in vivo study. Results: TRAP staining showed that shikimic acid significantly inhibited osteoclastogenesis and pit resorption in bone marrow monocytes and RAW264.7 cells, and actin ring formation assays showed that shikimic acid suppressed the bone resorption function of osteoclasts. Furthermore, shikimic acid inhibited the receptor activator of nuclear factor-κB RANK/tumor necrosis factor receptor-associated factor 6 (TRAF6) association, suppressed nuclear factor-κB and mitogen-activated protein kinase signaling pathways, and downregulated nuclear factor of activated T-cell cytoplasmic 1. The expression of osteoclastogenesis biomarkers, including TRAF6, calcitonin receptor, TRAP, cathepsin K, and matrix metalloproteinase-9, was inhibited. In vivo, shikimic acid also significantly ameliorated bone loss and prevented osteoclastogenesis in ovariectomized mice. Conclusion: Shikimic acid inhibited osteoclastogenesis and osteoclast function by blocking RANK ligand-induced recruitment of TRAF6, as well as downstream signaling pathways in vitro. Shikimic acid also reduced ovariectomy-induced osteoclastogenesis and bone loss in vivo.

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Deng, Yufeng, Weizhou Li, Yingying Zhang, Jingjing Li, Fangting He, Ke Dong, Zehui Hong, Ruocheng Luo i Xiaofang Pei. "α-Linolenic Acid Inhibits RANKL-Induced Osteoclastogenesis In Vitro and Prevents Inflammation In Vivo". Foods 12, nr 3 (3.02.2023): 682. http://dx.doi.org/10.3390/foods12030682.

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Inflammation is an important risk factor for bone-destroying diseases. Our preliminary research found that Zanthoxylum bungeanum seed oil (ZBSO) is abundant in unsaturated fatty acids and could inhibit osteoclastogenesis in receptor activator of nuclear factor κB ligand (RANKL)-induced RAW264.7 cells. However, the key constituents in ZBSO in the prevention of osteoclastogenesis and its possible mechanism related to inflammation are still unclear. Therefore, in this study, oleic acid (OA), linoleic acid (LA), palmitoleic acid (PLA), and alpha-linolenic acid (ALA) in ZBSO, havingthe strongest effect on RANKL-induced osteoclastogenesis, were selected by a tartrate-resistant acid phosphatase (TRAP) staining method. Furthermore, the effects of the selected fatty acids on anti-inflammation and anti-osteoclastogenesis in vitro and in vivo were assessed using RT-qPCR. Among the four major unsaturated fatty acids we tested, ALA displayed the strongest inhibitory effect on osteoclastogenesis. The increased expression of free fatty acid receptor 4 (FFAR4) and β-arrestin2 (βarr2), as well as the decreased expression of nuclear factor-kappa B (NF-κB), tumor necrosis factor-α (TNF-α), nuclear factor of activated T-cells c1 (NFATc1), and tartrate-resistant acid phosphatase (TRAP) in RAW264.7 cells after ALA treatment were observed. Moreover, in ovariectomized osteoporotic rats with ALA preventive intervention, we found that the expression of TNF-α, interleukin-6 (IL-6), interleukin-1β (IL-1β), NFATc1, and TRAP were decreased, while with the ALA therapeutic intervention, downregulated expression of NF-κB, NFATc1, TRAP, and transforming growth factor beta-activated kinase 1 (TAK1) were noticed. These results indicate that ALA, as the major unsaturated fatty acid in ZBSO, could inhibit RANKL-induced osteoclastogenesis via the FFAR4/βarr2 signaling pathway and could prevent inflammation, suggesting that ZBSO may be a promising potential natural product of unsaturated fatty acids and a dietary supplement for the prevention of osteoclastogenesis and inflammatory diseases.

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46

Huang, Hsuan-Ti, Tsung-Lin Cheng, Sung-Yen Lin, Cheng-Jung Ho, Joanna Y. Chyu, Rong-Sen Yang, Chung-Hwan Chen i Chwan-Li Shen. "Osteoprotective Roles of Green Tea Catechins". Antioxidants 9, nr 11 (16.11.2020): 1136. http://dx.doi.org/10.3390/antiox9111136.

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Osteoporosis is the second most common disease only secondary to cardiovascular disease, with the risk of fracture increasing with age. Osteoporosis is caused by an imbalance between osteoblastogenesis and osteoclastogenesis processes. Osteoclastogenesis may be enhanced, osteoblastogenesis may be reduced, or both may be evident. Inflammation and high reactive oxygen enhance osteoclastogenesis while reducing osteoblastogenesis by inducing osteoblast apoptosis and suppressing osteoblastic proliferation and differentiation. Catechins, the main polyphenols found in green tea with potent anti-oxidant and anti-inflammatory properties, can counteract the deleterious effects of the imbalance of osteoblastogenesis and osteoclastogenesis caused by osteoporosis. Green tea catechins can attenuate osteoclastogenesis by enhancing apoptosis of osteoclasts, hampering osteoclastogenesis, and prohibiting bone resorption in vitro. Catechin effects can be directly exerted on pre-osteoclasts/osteoclasts or indirectly exerted via the modulation of mesenchymal stem cells (MSCs)/stromal cell regulation of pre-osteoclasts through activation of the nuclear factor kB (RANK)/RANK ligand (RANKL)/osteoprotegerin (OPG) system. Catechins also can enhance osteoblastogenesis by enhancing osteogenic differentiation of MSCs and increasing osteoblastic survival, proliferation, differentiation, and mineralization. The in vitro effects of catechins on osteogenesis have been confirmed in several animal models, as well as in epidemiological observational studies on human subjects. Even though randomized control trials have not shown that catechins provide anti-fracture efficacy, safety data in the trials are promising. A large-scale, placebo-controlled, long-term randomized trial with a tea regimen intervention of optimal duration is required to determine anti-fracture efficacy.

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Kanzaki, H., M. Chiba, A. Sato, A. Miyagawa, K. Arai, S. Nukatsuka i H. Mitani. "Cyclical Tensile Force on Periodontal Ligament Cells Inhibits Osteoclastogenesis through OPG Induction". Journal of Dental Research 85, nr 5 (maj 2006): 457–62. http://dx.doi.org/10.1177/154405910608500512.

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The periodontal ligament (PDL) maintains homeostasis of periodontal tissue under mechanical tensile-loading caused by mastication. Occlusal load inhibits atrophic alveolar bone resorption. Previously, we discovered that continuous compressive force on PDL cells induced osteoclastogenesis-supporting activity, with up-regulation of RANKL. We hypothesized that, unlike compression, cyclical tensile force up-regulates OPG expression in PDL cells via TGF-beta up-regulation, and does not induce osteoclastogenesis-supporting activity. PDL cells were mechanically stimulated by cyclical tensile force in vitro. The conditioned media of PDL cells that had been subjected to cyclical tensile force inhibited osteoclastogenesis. Cyclical tensile force up-regulated not only RANKL mRNA expression, but also OPG mRNA expression in PDL cells. Tensile force up-regulated TGF-beta expression in PDL cells as well. Administration of neutralizing antibodies to TGF-beta inhibited OPG up-regulation under cyclical tensile-force stimulation in a dose-dependent manner. Additionally, the osteoclastogenesis-inhibitory effect of the conditioned media of PDL cells under cyclical tensile force was partially rescued by the administration of TGF-beta neutralizing antibodies. In conclusion, tensile force inhibited the osteoclastogenesis-supporting activity of PDL cells by inducing the up-regulation of OPG via TGF-beta stimulation.

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Swarnkar, Gaurav, Kannan Karuppaiah, Gabriel Mbalaviele, Tim (Hung-Po) Chen i Yousef Abu-Amer. "Osteopetrosis in TAK1-deficient mice owing to defective NF-κB and NOTCH signaling". Proceedings of the National Academy of Sciences 112, nr 1 (22.12.2014): 154–59. http://dx.doi.org/10.1073/pnas.1415213112.

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The MAP kinase TGFβ-activated kinase (TAK1) plays a crucial role in physiologic and pathologic cellular functions including cell survival, differentiation, apoptosis, inflammation, and oncogenesis. However, the entire repertoire of its mechanism of action has not been elucidated. Here, we found that ablation of Tak1 in myeloid cells causes osteopetrosis in mice as a result of defective osteoclastogenesis. Mechanistically, Tak1 deficiency correlated with increased NUMB-like (NUMBL) levels. Accordingly, forced expression of Numbl abrogated osteoclastogenesis whereas its deletion partially restored osteoclastogenesis and reversed the phenotype of Tak1 deficiency. Tak1 deletion also down-regulated Notch intracellular domain (NICD), but increased the levels of the transcription factor recombinant recognition sequence binding protein at Jκ site (RBPJ), consistent with NUMBL regulating notch signaling through degradation of NICD, a modulator of RBPJ. Accordingly, deletion of Rbpj partially corrected osteopetrosis in Tak1-deficient mice. Furthermore, expression of active IKK2 in RBPJ/TAK1-deficient cells significantly restored osteoclastogenesis, indicating that activation of NF-κB is essential for complete rescue of the pathway. Thus, we propose that TAK1 regulates osteoclastogenesis by integrating activation of NF-κB and derepression of NOTCH/RBPJ in myeloid cells through inhibition of NUMBL.

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Fukushima, Hidefumi, Akihiro Nakao, Fujio Okamoto, Masashi Shin, Hiroshi Kajiya, Seiji Sakano, Anna Bigas, Eijiro Jimi i Koji Okabe. "The Association of Notch2 and NF-κB Accelerates RANKL-Induced Osteoclastogenesis". Molecular and Cellular Biology 28, nr 20 (18.08.2008): 6402–12. http://dx.doi.org/10.1128/mcb.00299-08.

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ABSTRACT Notch signaling plays a key role in various cell differentiation processes including bone homeostasis. However, the specific involvement of Notch in regulating osteoclastogenesis is still controversial. In the present study, we show that RANKL induces expression of Jagged1 and Notch2 in bone marrow macrophages during osteoclast differentiation. Suppression of Notch signaling by a selective γ-secretase inhibitor or Notch2 short hairpin RNA suppresses RANKL-induced osteoclastogenesis. In contrast, induction of Notch signaling by Jagged1 or by ectopic expression of intracellular Notch2 enhances NFATc1 promoter activity and expression and promotes osteoclastogenesis. Finally, we found that Notch2 and p65 interact in the nuclei of RANKL-stimulated cells and that both proteins are recruited to the NFATc1 promoter, driving its expression. Taken together, our results show a new molecular cross talk between Notch and NF-κB pathways that is relevant in osteoclastogenesis.

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Zhang, Hong-Qi, Yun-Jia Wang, Guan-Teng Yang, Qi-Le Gao i Ming-Xing Tang. "Taxifolin Inhibits Receptor Activator of NF-κB Ligand-Induced Osteoclastogenesis of Human Bone Marrow-Derived Macrophages in vitro and Prevents Lipopolysaccharide-Induced Bone Loss in vivo". Pharmacology 103, nr 1-2 (6.12.2018): 101–9. http://dx.doi.org/10.1159/000495254.

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It has been reported that taxifolin inhibit osteoclastogenesis in RAW264.7 cells. In our research, the inhibition effects of taxifolin on the osteoclastogenesis of human bone marrow-derived macrophages (BMMs) induced by receptor activator of NF-κB ligand (RANKL) as well as the protection effects in lipopolysaccharide-induced bone lysis mouse model have been demonstrated. In vitro, taxifolin inhibited RANKL-induced osteoclast differentiation of human BMMs without cytotoxicity. Moreover, taxifolin significantly suppressed RANKL-induced gene expression, including tartrate-resistant acid phosphatase, matrix metalloproteinase-9 nuclear factor of activated T cells 1 and cathepsin K, and F-actin ring formation. Further studies showed that taxifolin inhibit osteoclastogenesis via the suppression of the NF-κB signaling pathway. In vivo, taxifolin prevented bone loss in mouse calvarial osteolysis model. In conclusion, the results suggested that taxifolin has a therapeutic potential for osteoclastogenesis-related diseases such as osteoporosis, osteolysis, and rheumatoid arthritis.

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