IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes
Elevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1β stimulated the expression of prostaglandin (PG) receptor EP4 via increased PGE2 production. However, the effect of IL-1β on osteoclast formation...
Saved in:
| Main Authors: | , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Wiley
2009-01-01
|
| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2009/308596 |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1832563255992647680 |
|---|---|
| author | Yusuke Watanabe Aki Namba Yukiko Aida Kazuhiro Honda Hideki Tanaka Naoto Suzuki Hideo Matsumura Masao Maeno |
| author_facet | Yusuke Watanabe Aki Namba Yukiko Aida Kazuhiro Honda Hideki Tanaka Naoto Suzuki Hideo Matsumura Masao Maeno |
| author_sort | Yusuke Watanabe |
| collection | DOAJ |
| description | Elevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1β stimulated the expression of prostaglandin (PG) receptor EP4 via increased PGE2 production. However, the effect of IL-1β on osteoclast formation via chondrocytes is unclear. Therefore, we examined the effect of IL-1β and/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-1β on 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-1β suppresses 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. |
| format | Article |
| id | doaj-art-f0e13bedbcb64e7482d6ff10f7db8389 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2009-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-f0e13bedbcb64e7482d6ff10f7db83892025-02-03T01:20:45ZengWileyMediators of Inflammation0962-93511466-18612009-01-01200910.1155/2009/308596308596IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in ChondrocytesYusuke Watanabe0Aki Namba1Yukiko Aida2Kazuhiro Honda3Hideki Tanaka4Naoto Suzuki5Hideo Matsumura6Masao Maeno7Nihon University Graduate School of Dentistry, Tokyo 101-8310, JapanNihon University Graduate School of Dentistry, Tokyo 101-8310, JapanDepartment of Fixed Prosthodontics, Nihon University School of Dentistry, 1-8-13, Kanda Surugadai, Chiyoda-ku, Tokyo 101-8310, JapanNihon University Graduate School of Dentistry, Tokyo 101-8310, JapanDepartment of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, JapanDepartment of Biochemistry, Nihon University School of Dentistry, Tokyo 101-8310, JapanDepartment of Fixed Prosthodontics, Nihon University School of Dentistry, 1-8-13, Kanda Surugadai, Chiyoda-ku, Tokyo 101-8310, JapanDepartment of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, JapanElevated interleukin (IL)-1 concentrations in synovial fluid have been implicated in joint bone and cartilage destruction. Previously, we showed that IL-1β stimulated the expression of prostaglandin (PG) receptor EP4 via increased PGE2 production. However, the effect of IL-1β on osteoclast formation via chondrocytes is unclear. Therefore, we examined the effect of IL-1β and/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-1β on 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-1β suppresses 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.http://dx.doi.org/10.1155/2009/308596 |
| spellingShingle | Yusuke Watanabe Aki Namba Yukiko Aida Kazuhiro Honda Hideki Tanaka Naoto Suzuki Hideo Matsumura Masao Maeno IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes Mediators of Inflammation |
| title | IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes |
| title_full | IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes |
| title_fullStr | IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes |
| title_full_unstemmed | IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes |
| title_short | IL-1β Suppresses the Formation of Osteoclasts by Increasing OPG Production via an Autocrine Mechanism Involving Celecoxib-Related Prostaglandins in Chondrocytes |
| title_sort | il 1β suppresses the formation of osteoclasts by increasing opg production via an autocrine mechanism involving celecoxib related prostaglandins in chondrocytes |
| url | http://dx.doi.org/10.1155/2009/308596 |
| work_keys_str_mv | AT yusukewatanabe il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT akinamba il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT yukikoaida il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT kazuhirohonda il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT hidekitanaka il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT naotosuzuki il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT hideomatsumura il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes AT masaomaeno il1bsuppressestheformationofosteoclastsbyincreasingopgproductionviaanautocrinemechanisminvolvingcelecoxibrelatedprostaglandinsinchondrocytes |