Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway
Wear debris-induced osteolysis, especially titanium (Ti) particles-induced osteolysis, is the most common cause of arthroplasty failure with no effective therapy. Previous studies have suggested that inflammation and impaired osteogenesis are associated with Ti particles -induced osteolysis. Seleniu...
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Frontiers Media S.A.
2023-07-01
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| Series: | Frontiers in Immunology |
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| Online Access: | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1171150/full |
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| author | Ruixuan Yu Yongjian Yuan Zhicheng Liu Zhicheng Liu Long Liu Zhaoning Xu Yunpeng Zhao Chunwang Jia Pengfei Zhang Hang Li Yuhao Liu Yi Wang Yi Wang Weiwei Li Lin Nie Xuecheng Sun Yuhua Li Ben Liu Haichun Liu |
| author_facet | Ruixuan Yu Yongjian Yuan Zhicheng Liu Zhicheng Liu Long Liu Zhaoning Xu Yunpeng Zhao Chunwang Jia Pengfei Zhang Hang Li Yuhao Liu Yi Wang Yi Wang Weiwei Li Lin Nie Xuecheng Sun Yuhua Li Ben Liu Haichun Liu |
| author_sort | Ruixuan Yu |
| collection | DOAJ |
| description | Wear debris-induced osteolysis, especially titanium (Ti) particles-induced osteolysis, is the most common cause of arthroplasty failure with no effective therapy. Previous studies have suggested that inflammation and impaired osteogenesis are associated with Ti particles -induced osteolysis. Selenium (Se) is an essential trace element in the human body, which forms selenomethionine (Se-Met) in nature, and selenoproteins has strong anti-inflammatory and antioxidant stress effects. In this study, the effects of Se-Met on Ti particles-induced osteolysis were observed and the potential mechanism was explored. We found that exogenous Se-Met relieved osteolysis induced by Ti particles in two animal models and MC3T3-E1 cells. We found that the addition of Se-Met effectively inhibited Ti particle-induced inflammation by regulating reactive oxygen species-dependent (ROS-dependent) NOD-like receptor protein 3 (NLRP3) inflammasome activation. These therapeutic effects were abrogated in MC3T3-E1 cells that had received a β-catenin antagonist, suggesting that Se-Met alleviates inflammatory osteolysis via the β-catenin signaling pathway. Collectively, these findings indicated that Se-Met may serve as a potential therapeutic agent for treating Ti particle-induced osteolysis. |
| first_indexed | 2024-03-12T22:49:50Z |
| format | Article |
| id | doaj.art-27893acee5bf4de1a55ffc3d5520c652 |
| institution | Directory Open Access Journal |
| issn | 1664-3224 |
| language | English |
| last_indexed | 2024-03-12T22:49:50Z |
| publishDate | 2023-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Immunology |
| spelling | doaj.art-27893acee5bf4de1a55ffc3d5520c6522023-07-20T12:59:28ZengFrontiers Media S.A.Frontiers in Immunology1664-32242023-07-011410.3389/fimmu.2023.11711501171150Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathwayRuixuan Yu0Yongjian Yuan1Zhicheng Liu2Zhicheng Liu3Long Liu4Zhaoning Xu5Yunpeng Zhao6Chunwang Jia7Pengfei Zhang8Hang Li9Yuhao Liu10Yi Wang11Yi Wang12Weiwei Li13Lin Nie14Xuecheng Sun15Yuhua Li16Ben Liu17Haichun Liu18Department of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaThe First Clinical Medical School, Shandong University, Jinan, Shandong, ChinaDepartment of Pathology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, ChinaSchool of Nursing and Rehabilitation, Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Plastic and Burns Surgery, The Second Hospital of Shandong University, Jinan, Shandong, ChinaEmergency Medicine Center, The Second Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Pathology, Qilu Hospital, Cheeloo College of Medicine, Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopedic Trauma, Weifang People’s Hospital, Weifang, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaDepartment of Orthopaedics, Qilu Hospital of Shandong University, Jinan, Shandong, ChinaWear debris-induced osteolysis, especially titanium (Ti) particles-induced osteolysis, is the most common cause of arthroplasty failure with no effective therapy. Previous studies have suggested that inflammation and impaired osteogenesis are associated with Ti particles -induced osteolysis. Selenium (Se) is an essential trace element in the human body, which forms selenomethionine (Se-Met) in nature, and selenoproteins has strong anti-inflammatory and antioxidant stress effects. In this study, the effects of Se-Met on Ti particles-induced osteolysis were observed and the potential mechanism was explored. We found that exogenous Se-Met relieved osteolysis induced by Ti particles in two animal models and MC3T3-E1 cells. We found that the addition of Se-Met effectively inhibited Ti particle-induced inflammation by regulating reactive oxygen species-dependent (ROS-dependent) NOD-like receptor protein 3 (NLRP3) inflammasome activation. These therapeutic effects were abrogated in MC3T3-E1 cells that had received a β-catenin antagonist, suggesting that Se-Met alleviates inflammatory osteolysis via the β-catenin signaling pathway. Collectively, these findings indicated that Se-Met may serve as a potential therapeutic agent for treating Ti particle-induced osteolysis.https://www.frontiersin.org/articles/10.3389/fimmu.2023.1171150/fullselenomethioninetitanium particle-induced osteolysisβ-catenininflammatory osteolysisNLRP3 |
| spellingShingle | Ruixuan Yu Yongjian Yuan Zhicheng Liu Zhicheng Liu Long Liu Zhaoning Xu Yunpeng Zhao Chunwang Jia Pengfei Zhang Hang Li Yuhao Liu Yi Wang Yi Wang Weiwei Li Lin Nie Xuecheng Sun Yuhua Li Ben Liu Haichun Liu Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway Frontiers in Immunology selenomethionine titanium particle-induced osteolysis β-catenin inflammatory osteolysis NLRP3 |
| title | Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway |
| title_full | Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway |
| title_fullStr | Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway |
| title_full_unstemmed | Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway |
| title_short | Selenomethionine against titanium particle-induced osteolysis by regulating the ROS-dependent NLRP3 inflammasome activation via the β-catenin signaling pathway |
| title_sort | selenomethionine against titanium particle induced osteolysis by regulating the ros dependent nlrp3 inflammasome activation via the β catenin signaling pathway |
| topic | selenomethionine titanium particle-induced osteolysis β-catenin inflammatory osteolysis NLRP3 |
| url | https://www.frontiersin.org/articles/10.3389/fimmu.2023.1171150/full |
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