ID | 58621 |
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Nakagawa, Saki
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences
Omori, Kazuhiro
Department of Periodontics and Endodontics, Okayama University Hospital
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Nakayama, Masaaki
Department of Oral Microbiology, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Mandai, Hiroki
Department of Medical Technology, School of Health Science, Gifu University of Medical Science
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Yamamoto, Satoshi
Department of Periodontics and Endodontics, Okayama University Hospital
Kobayashi, Hiroya
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama Universit
Sako, Hidefumi
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Sakaida, Kyosuke
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Yoshimura, Hiroshi
ivision of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
Ishii, Satoki
Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
Ibaragi, Soichiro
Department of Oral Maxillofacial Surgery, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Hirai, Kimito
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
Yamashiro, Keisuke
Department of Periodontics and Endodontics, Okayama University Hospital
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Yamamoto, Tadashi
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Suga, Seiji
Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University
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Takashiba, Shogo
Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University
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Abstract | 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)-κB 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 µM 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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Keywords | Synthetic (+)-terrein
Osteoclast
RANKL
NFATc1
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Published Date | 2020-06
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Publication Title |
International Immunopharmacology
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Volume | volume83
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Publisher | Elsevier
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Start Page | 106429
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ISSN | 1567-5769
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NCID | AA11516496
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Content Type |
Journal Article
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language |
English
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OAI-PMH Set |
岡山大学
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Copyright Holders | © 2020 The Authors.
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File Version | publisher
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DOI | |
Web of Science KeyUT | |
Related Url | isVersionof https://doi.org/10.1016/j.intimp.2020.106429
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License | http://creativecommons.org/licenses/by-nc-nd/4.0/
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Funder Name |
Japan Society for the Promotion of Science
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助成番号 | 16K11549
18K17069
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Open Access (Publisher) |
OA
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Open Archive (publisher) |
Non-OpenArchive
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