Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells
Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions d...
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| Format: | Article |
| Language: | English |
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Wiley
2015-01-01
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| Series: | Mediators of Inflammation |
| Online Access: | http://dx.doi.org/10.1155/2015/460310 |
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| author | Geng Yin Ying Wang Xiao-min Cen Min Yang Yan Liang Qi-bing Xie |
| author_facet | Geng Yin Ying Wang Xiao-min Cen Min Yang Yan Liang Qi-bing Xie |
| author_sort | Geng Yin |
| collection | DOAJ |
| description | Rheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions do not display significant clinical improvement after initiation of therapy. Thus, the relationship between inflammatory responses and RA therapy is still incompletely understood. In the present study, we proposed to determine whether enhanced inflammations may lead to cell apoptosis in rheumatoid arthritis synoviocytes. Our results indicated that products of lipid peroxidations, 4-HNE, may induce synovial intrinsic inflammations by activating NF-κB pathways and it may lead to cell apoptosis. Pharmacological inhibition of NF-κB activation may reduce the 4-HNE mediated inflammation responses and subsequent cell apoptosis. Our results may help to clarify the role of inflammations on RA development and imply that blocking NF-κB activation may be partly beneficial for human RA therapy. These findings might provide a mechanism-based rationale for developing new strategy to RA clinical therapy. |
| format | Article |
| id | doaj-art-4a5974e3ea534517a06565e6e10b84b2 |
| institution | Kabale University |
| issn | 0962-9351 1466-1861 |
| language | English |
| publishDate | 2015-01-01 |
| publisher | Wiley |
| record_format | Article |
| series | Mediators of Inflammation |
| spelling | doaj-art-4a5974e3ea534517a06565e6e10b84b22025-02-03T01:08:50ZengWileyMediators of Inflammation0962-93511466-18612015-01-01201510.1155/2015/460310460310Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial CellsGeng Yin0Ying Wang1Xiao-min Cen2Min Yang3Yan Liang4Qi-bing Xie5Department of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaDepartment of Rheumatology and Immunology, West China Hospital of Sichuan University, Chengdu, Sichuan 610041, ChinaRheumatoid arthritis (RA) is a systemic autoimmune disease characterized by chronic inflammation of multiple joints. The central pathogenesis of RA is the proliferation of synovial fibroblasts in response to inflammatory cytokines. However, some of the targeted therapies for inflammation reactions do not display significant clinical improvement after initiation of therapy. Thus, the relationship between inflammatory responses and RA therapy is still incompletely understood. In the present study, we proposed to determine whether enhanced inflammations may lead to cell apoptosis in rheumatoid arthritis synoviocytes. Our results indicated that products of lipid peroxidations, 4-HNE, may induce synovial intrinsic inflammations by activating NF-κB pathways and it may lead to cell apoptosis. Pharmacological inhibition of NF-κB activation may reduce the 4-HNE mediated inflammation responses and subsequent cell apoptosis. Our results may help to clarify the role of inflammations on RA development and imply that blocking NF-κB activation may be partly beneficial for human RA therapy. These findings might provide a mechanism-based rationale for developing new strategy to RA clinical therapy.http://dx.doi.org/10.1155/2015/460310 |
| spellingShingle | Geng Yin Ying Wang Xiao-min Cen Min Yang Yan Liang Qi-bing Xie Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells Mediators of Inflammation |
| title | Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells |
| title_full | Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells |
| title_fullStr | Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells |
| title_full_unstemmed | Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells |
| title_short | Lipid Peroxidation-Mediated Inflammation Promotes Cell Apoptosis through Activation of NF-κB Pathway in Rheumatoid Arthritis Synovial Cells |
| title_sort | lipid peroxidation mediated inflammation promotes cell apoptosis through activation of nf κb pathway in rheumatoid arthritis synovial cells |
| url | http://dx.doi.org/10.1155/2015/460310 |
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