Interleukin-6 and soluble interleukin-6 receptor suppress osteoclastic differentiation by inducing PGE2 production in chondrocytes
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This study examined how interleukin-6 (IL-6) and soluble IL-6 receptor (sIL-6r) influence osteoclastic differentiation through the function of chondrocytes. Chondrocytes were cultured with or without IL-6 and/or sIL-6r in the presence or absence of NS398, a specific inhibitor of cyclooxygenase (COX)-2, for up to 28 days. Chondrocytes were also cultured with or without IL-6 and sIL-6r for 28 days, and the conditioned medium from cells cultured without IL-6 and sIL-6r was used to induce differentiation of RAW264.7 cells into osteoclast precursors. Osteoclastic differentiation was assessed by tartrate-resistant acid phosphatase (TRAP) staining. Expression of osteoprotegerin (OPG), receptor activator of NF-κB ligand (RANKL), COX-2, and prostaglandin E(2) (PGE(2)) increased in cells exposed to IL-6 and sIL-6r, whereas expression of macrophage colony-stimulating factor (M-CSF) and bone resorption-related enzymes decreased. NS398 blocked the stimulatory/suppressive effects of IL-6 and sIL-6r on the expression of OPG, RANKL, and M-CSF. Fewer TRAP-positive multinucleated cells were detected after treatment with conditioned medium from IL-6- and sIL-6r-treated chondrocytes than after treatment with conditioned medium from untreated chondrocytes. These results suggest that IL-6 and sIL-6r interfere with osteoclast function through the involvement of chondrocytes. Specifically, they appear to suppress the differentiation of osteoclast precursors into osteoclasts by inducing chondrocytic PGE(2) production, which, in turn, increases OPG secretion and decreases M-CSF secretion by chondrocytes.
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IL-6 and its soluble receptor sIL-6r suppress differentiation of osteoclasts by inducing chondrocytic PGE2.
“He found that IL-6 and IL-6r suppressed the differentiation of osteoclasts by inducing chondrocytic PGE2 [44].”
From Osteoclasts and Microgravity (2020) · cites this paper as [44]
The Discussion concludes that IL-6 and sIL-6r may suppress osteoclast differentiation through PGE2 production in chondrocytes. The citing sentence presents this proposed causal mechanism as an established finding, whereas the paper frames it as a conclusion suggested by its results. (LLM, conf=0.78)
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- Watanabe Y, Namba A, Aida Y, Honda K, Tanaka H, Suzuki N, Matsumura H, Maeno M (2010) IL- 1β suppresses the formation of osteoclasts by increasing OPG production via an autocrine m e c h a n i s m i nvo l v i n g c e l e c o x i b -r e l a t e d prostaglandins in chondrocytes. Mediators Inflamm 2009, doi:10.1155/2009/308596. · DOI · Paper page
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Smith, J. K. (2020) · Life · doi:10.3390/life10090207 · Cited by 52 · see citing works
- Authors
- Honda, K.
- Affiliations
- Nihon University (JP)
- Corresponding author
- Honda, Kazuhiro
- Venue
- Journal of Oral Science
- Publisher
- Nihon University School of Dentistry
- Published
- 2011
- Volume
- 53
- Issue
- 1
- Pages
- 87-96
- ISSN
- 1343-4934 (ISSN-L)
- 1880-4926
- OpenAlex
- W2131773419
- Cited by
- 15
- References
- 0
- Citations by year
- 2023: 1 · 2022: 2 · 2020: 1 · 2018: 2 · 2016: 1 · 2015: 1 · 2014: 1 · 2013: 2 · 2012: 4
- FWCI
- 0.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Oral Science (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Nihon University
- School of Dentistry, Nihon University
- Promotion and Mutual Aid Corporation for Private Schools of Japan
- 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
- interleukin-6, soluble IL-6 receptor, osteoclastogenesis, chondrocytes, prostaglandin E2, cyclooxygenase-2, osteoprotegerin, RANKL, macrophage colony-stimulating factor, bone resorption, osteoclast precursors, TRAP staining
- MeSH terms
- Interleukin-6 Inhibitors, Anti-Inflammatory Agents, Non-Steroidal, Bone Resorption, Cell Differentiation, Cells, Cultured, Humans, Nitrobenzenes, Osteoclasts, Prostaglandin-Endoperoxide Synthases, Sulfonamides, Dinoprostone, Interleukin-6, Gene Expression, Macrophage Colony-Stimulating Factor, Chondrocytes, Receptors, Interleukin-6, Matrix Metalloproteinase 9, Carbonic Anhydrase II, Cyclooxygenase 2, Osteoprotegerin, RANK Ligand, Cathepsin K
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