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• W2007102118 abstract "Objective: The protein tyrosine phosphatase, TC-PTP, is known to de-phosphorylate STAT3 and inhibit its activity in vitro. STAT3 is activated in response to IL-6 family ligands, among other pathways. We sought to determine the regulation and potential biological consequences of TC-PTP expression using in vivo models of sepsis, endotoxemia and chronic inflammation associated with cancer cachexia. Methods: TC-PTP expression was measured in cell lines treated with IL-6, and in tissues from normal, IL-6 treated, septic, endotoxemic or cachectic mice. STAT3 activation and expression of acute phase response genes was measured in the human hepatoma cell line, HepG2, treated with IL-6 and/or with recombinant adenovirus expressing TC-PTP and GFP or GFP alone. Results: Hela cells treated with IL-6 showed increased expression of TC-PTP. In mice, systemic administration of IL-6 robustly induced TC-PTP protein in the liver. TC-PTP was also induced in lung, kidney, fat and muscle. Peak TC-PTP expression was followed by a gradual decrease in STAT3 phosphorylation and diminished expression acute phase genes. In two models of sepsis/endotoxemia, namely chronic LPS administration and cecal ligation and puncture (CLP), TC-PTP was greatly induced. Endogenous IL-6 was largely responsible for TC-PTP expression, because septic/endotoxemic il6 null mice showed no hepatic TC-PTP induction. TC-PTP expression may be a feature of many inflammatory diseases, as it was also induced in the liver in models of advanced cancer, including colon-26 adenoma and B16F10 melanoma tumor-bearing mice. TC-PTP may function to limit STAT3 activity as infection of human hepatic adenoma cell line HepG2 with recombinant TC-PTP adenovirus blocked IL-6 induced STAT3 phosphorylation and expression of acute phase response genes. Furthermore, IL-6 stimulation of cells transfected with a TC-PTP promoter / luciferase construct indicate direct IL-6 responsiveness. Conclusions: IL-6 induces TC-PTP expression, potentially through transcriptional induction by STAT3. TC-PTP expression results in decreased STAT3 activity. Therefore TC-PTP may function as a feed-back inhibitor of IL-6’s in vivo effects, including the induction of the acute phase response. These studies implicate TC-PTP in the pathophysiology of inflammatory disease, including sepsis and cancer cachexia. Thus, modulating TC-PTP may be a mechanism for inhibiting STAT3 activation in chronic inflammatory states including severe infection, cancer and diabetes." @default.
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• W2007102118 date "2008-02-01" @default.
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• W2007102118 title "QS380. TC-PTP Feedback Inhibits IL-6 Activation of the Hepatic Acute Phase Response" @default.
• W2007102118 doi "https://doi.org/10.1016/j.jss.2007.12.634" @default.
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