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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/112517

    Title: Myostatin induces tumor necrosis factor-α expression in rheumatoid arthritis synovial fibroblasts through the PI3K-Akt signaling pathway
    Authors: Su, Chen?Ming;Su, Chen?Ming;Hu, Sung?Lin;Hu, Sung?Lin;Sun, Yi;Sun, Yi;Zhao, Jin;Zhao, Jin;Da, Chengqian;Dai, Chengqian;Wang, Lihong;Wang, Lihong;Xu, Guohong;Xu, Guohong;湯智昕;Chih-Hsin;Tang
    Contributors: 生物科技學系
    Date: 2019-06
    Issue Date: 2019-11-15 10:47:46 (UTC+8)
    Abstract: In rheumatoid arthritis (RA), a chronic inflammatory disease, loss of muscle mass is an important contributor to the loss of muscle strength in RA patients. Myostatin, a myokine involved in the process of muscle hypertrophy and myogenesis, enhances osteoclast differentiation and inflammation. Here, we investigated the mechanisms of myostatin in RA synovial inflammation. We found a positive correlation between myostatin and tumor necrosis factor-α (TNF-α), a well-known proinflammatory cytokine, in RA synovial tissue. Our in vitro results also showed that myostatin dose-dependently induced TNF-α expression through the phosphatidylinositol 3-kinase (PI3K)-Akt-AP-1 signaling pathway. Myostatin treatment of human MH7A cells stimulated AP-1-induced luciferase activity and activation of the c-Jun binding site on the TNF-α promoter. Our results indicated that myostatin increases TNF-α expression via the PI3K-Akt-AP-1 signaling pathway in human RA synovial fibroblasts. Myostatin appears to be a promising target in RA therapy.
    Appears in Collections:[生物科技學系] 期刊論文

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