Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells
Oxidative stress within the arthritis joint has been indicated to be involved in generating mediators for tissue degeneration and inflammation. COX‐2 is a mediator in inflammatory action, pain and some catabolic reactions in inflamed tissues. Here, we demonstrated a direct relationship between oxida...
| Main Authors: | , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
Wiley
2015-01-01
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| Series: | FEBS Open Bio |
| Subjects: | |
| Online Access: | https://doi.org/10.1016/j.fob.2015.06.001 |
| _version_ | 1811206031291711488 |
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| author | Yuta Onodera Takeshi Teramura Toshiyuki Takehara Kanae Shigi Kanji Fukuda |
| author_facet | Yuta Onodera Takeshi Teramura Toshiyuki Takehara Kanae Shigi Kanji Fukuda |
| author_sort | Yuta Onodera |
| collection | DOAJ |
| description | Oxidative stress within the arthritis joint has been indicated to be involved in generating mediators for tissue degeneration and inflammation. COX‐2 is a mediator in inflammatory action, pain and some catabolic reactions in inflamed tissues. Here, we demonstrated a direct relationship between oxidative stress and Cox‐2 expression in the bovine synovial fibroblasts. Furthermore, we elucidated a novel mechanism, in which oxidative stress induced phosphorylation of MAPKs and NF‐κB through TAK1 activation and resulted in increased Cox‐2 and prostaglandin E2 expression. Finally, we demonstrated that ROS‐induced Cox‐2 expression was inhibited by supplementation of an antioxidant such as N‐acetyl cysteamine and hyaluronic acidin vitro andin vivo. From these results, we conclude that oxidative stress is an important factor for generation of Cox‐2 in synovial fibroblasts and thus its neutralization may be an effective strategy in palliative therapy for chronic joint diseases. |
| first_indexed | 2024-04-12T03:40:43Z |
| format | Article |
| id | doaj.art-30849c63087f4e53b94bc872c704381b |
| institution | Directory Open Access Journal |
| issn | 2211-5463 |
| language | English |
| last_indexed | 2024-04-12T03:40:43Z |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | FEBS Open Bio |
| spelling | doaj.art-30849c63087f4e53b94bc872c704381b2022-12-22T03:49:17ZengWileyFEBS Open Bio2211-54632015-01-015149250110.1016/j.fob.2015.06.001Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cellsYuta Onodera0Takeshi Teramura1Toshiyuki Takehara2Kanae Shigi3Kanji Fukuda4Division of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, JapanDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, JapanDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, JapanDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, JapanDivision of Cell Biology for Regenerative Medicine, Institute of Advanced Clinical Medicine, Kindai University Faculty of Medicine, Osaka, JapanOxidative stress within the arthritis joint has been indicated to be involved in generating mediators for tissue degeneration and inflammation. COX‐2 is a mediator in inflammatory action, pain and some catabolic reactions in inflamed tissues. Here, we demonstrated a direct relationship between oxidative stress and Cox‐2 expression in the bovine synovial fibroblasts. Furthermore, we elucidated a novel mechanism, in which oxidative stress induced phosphorylation of MAPKs and NF‐κB through TAK1 activation and resulted in increased Cox‐2 and prostaglandin E2 expression. Finally, we demonstrated that ROS‐induced Cox‐2 expression was inhibited by supplementation of an antioxidant such as N‐acetyl cysteamine and hyaluronic acidin vitro andin vivo. From these results, we conclude that oxidative stress is an important factor for generation of Cox‐2 in synovial fibroblasts and thus its neutralization may be an effective strategy in palliative therapy for chronic joint diseases.https://doi.org/10.1016/j.fob.2015.06.001Reactive oxygen speciesCox-2TAK1Synovial tissuesOA model |
| spellingShingle | Yuta Onodera Takeshi Teramura Toshiyuki Takehara Kanae Shigi Kanji Fukuda Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells FEBS Open Bio Reactive oxygen species Cox-2 TAK1 Synovial tissues OA model |
| title | Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells |
| title_full | Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells |
| title_fullStr | Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells |
| title_full_unstemmed | Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells |
| title_short | Reactive oxygen species induce Cox‐2 expression via TAK1 activation in synovial fibroblast cells |
| title_sort | reactive oxygen species induce cox 2 expression via tak1 activation in synovial fibroblast cells |
| topic | Reactive oxygen species Cox-2 TAK1 Synovial tissues OA model |
| url | https://doi.org/10.1016/j.fob.2015.06.001 |
| work_keys_str_mv | AT yutaonodera reactiveoxygenspeciesinducecox2expressionviatak1activationinsynovialfibroblastcells AT takeshiteramura reactiveoxygenspeciesinducecox2expressionviatak1activationinsynovialfibroblastcells AT toshiyukitakehara reactiveoxygenspeciesinducecox2expressionviatak1activationinsynovialfibroblastcells AT kanaeshigi reactiveoxygenspeciesinducecox2expressionviatak1activationinsynovialfibroblastcells AT kanjifukuda reactiveoxygenspeciesinducecox2expressionviatak1activationinsynovialfibroblastcells |