ArticleInternational journal of molecular sciences2020
TGFβ1 Regulates Human RANKL-Induced Osteoclastogenesis via Suppression of NFATc1 Expression.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.
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Who cites it
26 citing papers in PubMed, 31 citations in OpenAlex.
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- Immune-Guided Bone Healing: The Role of Osteoimmunity in Tissue Engineering Approaches.International journal of molecular sciences · 2025Review
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- Recent advances in the multifaceted mechanisms of catalpol in treating osteoporosis.Frontiers in pharmacology · 2025Review
- A new direction in periodontitis treatment: biomaterial-mediated macrophage immunotherapy.Journal of nanobiotechnology · 2024Review
- Local application of zoledronate inhibits early bone resorption and promotes bone formation.JBMR plus · 2024Article
- Identification and validation of iron metabolism genes in osteoporosis.BMC medical genomics · 2024Article
- Cinnamaldehyde attenuates streptozocin-induced diabetic osteoporosis in a rat model by modulating netrin-1/DCC-UNC5B signal transduction.Frontiers in pharmacology · 2024Article
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- SIRT2 regulates extracellular vesicle-mediated liver-bone communication.Nature metabolism · 2023Article
- Bone Cell Exosomes and Emerging Strategies in Bone Engineering.Biomedicines · 2022Review
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- Alginate oligosaccharide alleviates senile osteoporosis via the RANKL-RANK pathway in D-galactose-induced C57BL/6J mice.Chemical biology & drug design · 2022Article
- Effect of Enamel Matrix Derivatives on Osteoclast Formation from PBMC of Periodontitis Patients and Healthy Individuals after Interaction with Activated Endothelial Cells.Medicina (Kaunas, Lithuania) · 2021Article
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Authors and funding
9 authors at 1 institution in 1 country.
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Abstract
Osteoclasts are multinucleated giant cells responsible for bone resorption. Various mediators involved in osteoclast differentiation have been investigated as possible therapeutic targets for osteoporosis and rheumatoid arthritis (RA). Although transforming growth factor beta1 (TGFβ1) has been described as one such multifunctional cytokine essential for bone remodeling, its effect on osteoclastogenesis remains controversial. Therefore, we sought to examine the effect of TGFβ1 on osteoclast generation induced by receptor activator of nuclear factor (NF)-κB ligand (RANKL) in humans. Peripheral blood monocytes, isolated using magnetic bead sorting, were cultured with macrophage-colony stimulating factor (M-CSF) or RANKL with or without TGFβ1. Tartrate-resistant acid phosphatase (TRAP) staining, as well as bone resorption assays, revealed that TGFβ1 suppressed RANKL-mediated human osteoclast development. Real-time reverse transcription PCR and Western blotting revealed that TGFβ1 reduced the gene and protein expression of nuclear factor of activated T cells, cytoplasmic 1 (NFATc1), the master regulator of osteoclast differentiation, respectively. Luciferase assays indicated that TGFβ1 inhibited the NF-κB p65-stimulated promoter activity of NFATc1. Immunofluorescence analysis demonstrated that TGFβ1 abrogated RANKL-induced nuclear translocation of p65. Thus, TGFβ1 regulates human RANKL-induced osteoclastogenesis via downregulation of NFATc1 by blocking nuclear translocation of NF-κB, suggesting that TGFβ1 may be a potential therapeutic target for RA.
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