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Cited by 13Bone Metabolism and DiseasesOsteoarthritis Treatment and MechanismsRheumatoid Arthritis Research and Therapies

IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes

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Watanabe, Yusuke, Namba, Aki, Aida, Yukiko, Honda, Kazuhiro, Tanaka, Hideki, Suzuki, Naoto, Matsumura, Hideo, Maeno, Masao·2009·Mediators of Inflammation
DOI 10.1155/2009/308596PMC PMC2829618
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Abstract

Elevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1βstimulated the expression of prostaglandin (PG) receptor EP4 via increasedPGE2production. However, the effect of IL-1βon osteoclast formation via chondrocytes is unclear. Therefore, we examined the effect of IL-1βand/or celecoxib on the expression of macrophage colony-stimulating factor (M-CSF), receptor activator of NF-κB ligand (RANKL), and osteoprotegerin (OPG) in human chondrocytes, and the indirect effect of IL-1βon osteoclast-like cell formation using RAW264.7 cells. OPG and RANKL expression increased with IL-1β; whereas M-CSF expression decreased. Celecoxib blocked the stimulatory effect of IL-1β. Conditioned medium from IL-1β-treated chondrocytes decreased TRAP staining in RAW264.7 cells. These results suggest that IL-1βsuppresses the formation of osteoclast-like cells via increased OPG production and decreased M-CSF production in chondrocytes, and OPG production may increase through an autocrine mechanism involving celecoxib-related PGs.

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  • IL-1β has also been reported to suppress osteoclast formation by upregulating OPG production by chondrocytes.

    “However, IL-1β has also been reported to suppress osteoclast formation by upregulating OPG production by chondrocytes [34].”

    From Osteoclasts and Microgravity (2020) · cites this paper as [34]

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Research works printed but not linked: 36

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Authors
Watanabe, Y., Namba, A., Aida, Y., Honda, K., Tanaka, H., Suzuki, N., Matsumura, H., & Maeno, M.
Affiliations
Nihon University (JP)
Corresponding author
Aida, Yukiko
ORCID
Venue
Mediators of Inflammation
Publisher
Wiley
Published
2009
Volume
2009
Pages
1-9
ISSN
  • 0962-9351 (ISSN-L)
  • 1466-1861
DOI
10.1155/2009/308596
PMC
PMC2829618
OpenAlex
W2147227779
Cited by
13
References
0
Citations by year
2026: 1 · 2021: 1 · 2020: 1 · 2019: 1 · 2017: 1 · 2014: 2 · 2012: 3
FWCI
0.81
Type
journal article
Language
en
Open access
Licence
Locations
  • Mediators of Inflammation (publishedVersion, cc-by)
  • Europe PMC (PubMed Central) (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Japan Society for the Promotion of Science (19592182, 19791384)
  • Nihon University (19592182, 19791384)
Topics
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Bone Metabolism and Diseases
  • Health Sciences › Medicine › Rheumatology › Osteoarthritis Treatment and Mechanisms
  • Health Sciences › Medicine › Rheumatology › Rheumatoid Arthritis Research and Therapies
Keywords
IL-1β, osteoclastogenesis, osteoprotegerin, chondrocytes, celecoxib, prostaglandins, prostaglandin E2, EP4 receptor, macrophage colony-stimulating factor, RANKL, autocrine signaling, osteoclast-like cells, synovial fluid
MeSH terms
Celecoxib, Animals, Base Sequence, Cell Differentiation, Cell Line, Cells, Cultured, Humans, Osteoclasts, Prostaglandins, Pyrazoles, Sulfonamides, Dinoprostone, Gene Expression, Macrophage Colony-Stimulating Factor, Culture Media, Conditioned, DNA Primers, Inflammation Mediators, Autocrine Communication, Chondrocytes, Mice, Osteoprotegerin, RANK Ligand, Interleukin-1beta

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