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| 題名: | FAK Activation Is Required for TNF-a-Induced IL-6 Production in Myoblasts |
| 作者: | Tseng, Wen-Pei;Su, Chen-Ming;Tang, Chih-Hsin |
| 貢獻者: | 運動健康所 |
| 日期: | 2010-05
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| 上傳時間: | 2014-01-15T04:02:52Z
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| 出版者: | Wiley-Liss, Hoboken, NJ, ETATS-UNIS |
| 摘要: | Tumor necrosis factor-alpha (TNF-alpha) is a pleiotropic cytokine produced by activated macrophages. IL-6 is a multifunctional cytokine that plays a central role in both innate and acquired immune responses. We investigated the signaling pathway involved in IL-6 production stimulated by TNF-alpha in cultured myoblasts. TNF-alpha caused concentration-dependent increases in IL-6 production. TNF-alpha-mediated IL-6 production was attenuated by focal adhesion kinase (FAK) mutant and siRNA. Pretreatment with phosphatidylinositol 3-kinase inhibitor (PI3K; Ly294002 and wortmannin), Akt inhibitor, NF-kappaB inhibitor (pyrrolidine dithiocarbamate, PDTC), and IkappaB protease inhibitor (L-1-tosylamido-2-phenyl phenylethyl chloromethyl ketone, TPCK) also inhibited the potentiating action of TNF-alpha. TNF-alpha increased the FAK, PI3K, and Akt phosphorylation. Stimulation of myoblasts with TNF-alpha activated IkappaB kinase alpha/beta (IKKalpha/beta), IkappaBalpha phosphorylation, p65 phosphorylation, and kappaB-luciferase activity. TNF-alpha mediated an increase of kappaB-luciferase activity which was inhibited by Ly294002, wortmannin, Akt inhibitor, PDTC and TPCK or FAK, PI3K, and Akt mutant. Our results suggest that TNF-alpha increased IL-6 production in myoblasts via the FAK/PI3K/Akt and NF-kappaB signaling pathway. |
| 關聯: | Journal of Cellular Physiology, 223(2): 389-396 |
| 顯示於類別: | [運動健康研究所] 期刊論文
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