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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 ORCID Kaken ID publons researchmap
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 ORCID Kaken ID publons researchmap
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 ORCID Kaken ID publons researchmap
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 ORCID Kaken ID publons
Yamamoto, Tadashi Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University ORCID Kaken ID publons researchmap
Suga, Seiji Division of Applied Chemistry, Graduate School of Natural Sciences and Technology, Okayama University ORCID Kaken ID researchmap
Takashiba, Shogo Department of Pathophysiology-Periodontal Science, Graduate School of Medicine, Dentistry and Pharmaceutical Sciences, Okayama University ORCID Kaken ID publons researchmap
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.
Keywords
Synthetic (+)-terrein
Osteoclast
RANKL
NFATc1
Published Date
2020-06
Publication Title
International Immunopharmacology
Volume
volume83
Publisher
Elsevier
Start Page
106429
ISSN
1567-5769
NCID
AA11516496
Content Type
Journal Article
language
英語
OAI-PMH Set
岡山大学
Copyright Holders
© 2020 The Authors.
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publisher
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DOI
Web of Science KeyUT
Related Url
isVersionof https://doi.org/10.1016/j.intimp.2020.106429
License
http://creativecommons.org/licenses/by-nc-nd/4.0/
Funder Name
Japan Society for the Promotion of Science
助成番号
16K11549
18K17069
Open Access (Publisher)
OA
Open Archive (publisher)
Non-OpenArchive