Role and Regulation of Transcription Factors in Osteoclastogenesis

Jiang, Tao; Xia, Tianshuang; Qiao, Fangliang; Wang, Nani; Jiang, Yiping; Xin, Hailiang

doi:10.3390/ijms242216175

Cited by 10 publications

(2 citation statements)

References 243 publications

(302 reference statements)

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“…Osteoclastogenesis is derived from BMMs and is induced by macrophage colony-stimulating factor ( M-CSF ) and RANKL ( Søe et al, 2021 ). c-Fos is an indispensable transcription factor in RANKL-induced osteoclastogenesis ( Jiang et al, 2023 ). In the treatment of different etiology-induced bone loss models, drugs are mainly used by inhibiting the RANKL-induced c-Fos signaling pathway and the attenuation of osteoclast-specific genes, such as TRAP and CTSK ( Kwak et al, 2019 ; Zhao et al, 2020 ).…”

Section: Discussionmentioning

confidence: 99%

Oligomeric proanthocyanidins ameliorates osteoclastogenesis through reducing OPG/RANKL ratio in chicken's embryos

Yu,

Fu,

Gong

et al. 2024

Poultry Science

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Section: Discussionmentioning

confidence: 99%

Oligomeric proanthocyanidins ameliorates osteoclastogenesis through reducing OPG/RANKL ratio in chicken's embryos

Yu,

Fu,

Gong

et al. 2024

Poultry Science

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“… 142 Mice lacking NF‐κB p50 and p52 exhibit notable dwarfism, thickened hypertrophic chondrocyte layers, severe osteopetrosis, and a lack of osteoclasts. 143 Whereas NF‐κB activation in osteoblasts can either stimulate or inhibit osteogenesis. For example, TNF‐induced NF‐κB activation suppresses bone formation by obstructing RUNX2, thus interfering with BMP signaling.…”

Section: Signaling Pathways and Molecules In Bone Homeostasismentioning

confidence: 99%

Regulation of bone homeostasis: signaling pathways and therapeutic targets

Wu,

Li,

Jiang

et al. 2024

MedComm

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As a highly dynamic tissue, bone is continuously rebuilt throughout life. Both bone formation by osteoblasts and bone resorption by osteoclasts constitute bone reconstruction homeostasis. The equilibrium of bone homeostasis is governed by many complicated signaling pathways that weave together to form an intricate network. These pathways coordinate the meticulous processes of bone formation and resorption, ensuring the structural integrity and dynamic vitality of the skeletal system. Dysregulation of the bone homeostatic regulatory signaling network contributes to the development and progression of many skeletal diseases. Significantly, imbalanced bone homeostasis further disrupts the signaling network and triggers a cascade reaction that exacerbates disease progression and engenders a deleterious cycle. Here, we summarize the influence of signaling pathways on bone homeostasis, elucidating the interplay and crosstalk among them. Additionally, we review the mechanisms underpinning bone homeostatic imbalances across diverse disease landscapes, highlighting current and prospective therapeutic targets and clinical drugs. We hope that this review will contribute to a holistic understanding of the signaling pathways and molecular mechanisms sustaining bone homeostasis, which are promising to contribute to further research on bone homeostasis and shed light on the development of targeted drugs.

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Molecular Mechanisms of Curdlan‐Induced Suppression of NFATc1 Expression in Osteoclasts

Koga,

Nagai‐Yoshioka,

Yamasaki

et al. 2024

J of Cellular Biochemistry

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Osteoclasts derived from hematopoietic stem cells express immunoreceptors on their cell surface. Previously, we showed that the β‐glucan curdlan suppressed osteoclastogenesis via binding to dectin‐1, a pattern recognition receptor. Curdlan negatively regulates osteoclast differentiation and bone resorption capacity by suppressing the expression of nuclear factor of activated T cells 1 (NFATc1), a master factor for osteoclast differentiation, in a dectin‐1‐dependent manner; however, the mechanism involved in this process has not yet been fully elucidated. In this study, we aimed to elucidate the molecular mechanism involved in the suppression of RANKL‐induced osteoclast differentiation by curdlan. Real‐time RT‐qPCR results showed that curdlan suppressed the expression of NFATc1 in cells of the osteoclast progenitor cell line RAW264.7 overexpressing dectin‐1 (d‐RAW cells), without altering the expression of negative regulators. Therefore, we examined the effect of curdlan on the NF‐κB pathway, which is important for the induction of NFATc1 expression. Western blot analysis results showed that curdlan addition suppressed RANKL‐induced NF‐κB activation in the vector control line (c‐RAW) cells with low expression of dectin‐1, in d‐RAW cells, and the parental RAW264.7 (RAW) cells. The results of tartrate‐resistant alkaline phosphatase staining and real‐time RT‐qPCR showed that curdlan addition suppressed osteoclast differentiation in RAW cells, suggesting the presence of a dectin‐1‐independent modification system. Finally, we focused on the complement receptor 3 (CR3), which binds β‐glucan, and revealed that blocking the binding of β‐glucan to the CD11b molecule, a component of CR3, by neutralizing antibody, recovered the suppression of IκBα degradation by curdlan. These results suggest that the suppression of osteoclast differentiation by curdlan involves not only the dectin‐1‐dependent pathway but also the negative regulation of NFATc1 via modification of the NF‐κB pathway via CR3 recognition. The results of this study may aid to establish treatment methods for metabolic bone diseases and inflammatory bone destruction and to clarify their pathogenesis.

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Role and Regulation of Transcription Factors in Osteoclastogenesis

Cited by 10 publications

References 243 publications

Oligomeric proanthocyanidins ameliorates osteoclastogenesis through reducing OPG/RANKL ratio in chicken's embryos

Oligomeric proanthocyanidins ameliorates osteoclastogenesis through reducing OPG/RANKL ratio in chicken's embryos

Regulation of bone homeostasis: signaling pathways and therapeutic targets

Molecular Mechanisms of Curdlan‐Induced Suppression of NFATc1 Expression in Osteoclasts

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