Journal
INTERNATIONAL IMMUNOPHARMACOLOGY
Volume 83, Issue -, Pages -Publisher
ELSEVIER
DOI: 10.1016/j.intimp.2020.106429
Keywords
Synthetic (+)-terrein; Osteoclast; RANKL; NFATc1
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Funding
- Japan Society for the Promotion of Science, Ryobi Memorial Foundation [16K11549, 18K17069]
- Wesco Scientific Promotion Foundation
- Grants-in-Aid for Scientific Research [18K17069, 16K11549] Funding Source: KAKEN
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Pathophysiological bone resorption is commonly associated with periodontal disease and involves the excessive resorption of bone matrix by activated osteoclasts. Receptor activator of nuclear factor (NF)-kappa B ligand (RANKL) signaling pathways have been proposed as targets for inhibiting osteoclast differentiation and bone resorption. The fungal secondary metabolite (+)-terrein is a natural compound derived from Aspergillus terreus that has previously shown anti-interleukin-6 properties related to inflammatory bone resorption. However, its effects and molecular mechanism of action on osteoclastogenesis and bone resorption remain unclear. In the present study, we showed that 10 mu M synthetic (+)-terrein inhibited RANKL-induced osteoclast formation and bone resorption in a dose-dependent manner and without cytotoxicity. RANKL-induced messenger RNA expression of osteoclast-specific markers including nuclear factor of activated T-cells cytoplasmic 1 (NFATc1), the master regulator of osteoclastogenesis, cathepsin K, tartrate-resistant acid phosphatase (Trap) was completely inhibited by synthetic (+)-terrein treatment. Furthermore, synthetic (+)-terrein decreased RANKL-induced NFATc1 protein expression. This study revealed that synthetic (+)-terrein attenuated osteoclast formation and bone resorption by mediating RANKL signaling pathways, especially NFATc1, and indicated the potential effect of (+)-terrein on inflammatory bone resorption including periodontal disease.
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