FAK activation is required for TNF-α-induced IL-6 production in myoblasts

Wen Pei Tseng, Chen Ming Su, Chih Hsin Tang

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21 Citations (Scopus)

Abstract

Tumor necrosis factor-α (TNF-α) 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-α in cultured myoblasts. TNF-α caused concentration-dependent increases in IL-6 production. TNF-α-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-κb inhibitor (pyrrolidine dithiocarbamate, pdtc), and iκb protease inhibitor (l-1-tosylamido-2-phenyl phenylethyl chloromethyl ketone, tpck) also inhibited the potentiating action of tnf-α. Tnf-α increased the fak, pi3k, and akt phosphorylation. Stimulation of myoblasts with tnf-α activated iκb kinase α/β (ikkα/β), iκbα phosphorylation, p65 phosphorylation, and κb-luciferase activity. Tnf-α mediated an increase of κb-luciferase activity which was inhibited by ly294002, wortmannin, akt inhibitor, pdtc and tpck or fak, pi3k, and akt mutant. Our results suggest that tnf-α increased il-6 production in myoblasts via the fak/pi3k/akt and nf-κb signaling pathway.

Original languageEnglish
Pages (from-to)389-396
Number of pages8
JournalJournal of Cellular Physiology
Volume223
Issue number2
DOIs
Publication statusPublished - 2010 May 1

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All Science Journal Classification (ASJC) codes

  • Physiology
  • Clinical Biochemistry
  • Cell Biology

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