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10.1016/j.freeradbiomed.2013.09.027 http://scihub22266oqcxt.onion/10.1016/j.freeradbiomed.2013.09.027 C4798239!4798239 !24095726     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=24095726 &cmd=llinks): Failed to open stream: HTTP request failed! 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A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine |pdf=|usr=}}{{24095726 }} gab.com Text A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine JO: Free Radic Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=24095726 #FOAvip Nicotine stimulates the cholinergic anti-inflammatory pathway and prevents excessive inflammation by inhibiting the release of inflammatory cytokines from macrophages. We have previously reported that heme oxygenase-1 (HO-1) and tristetraprolin (TTP) are induced by nicotine and mediate the anti-inflammatory function of nicotine in macrophages. However, it was not clear whether the two molecules are functionally linked. In this study, we sought to determine whether HO-1 associates with TTP to mediate the anti-inflammatory effects of nicotine. Inhibition of HO-1 activity or HO-1 expression attenuated the effects of nicotine on STAT3 activation, TTP induction, and TNF-? production in LPS-treated macrophages. Induction of HO-1 expression increased the level of TTP in the absence of nicotine. In an LPS-induced endotoxemia model, HO-1 deficiency blocked the effects of nicotine on the STAT3 phosphorylation, TTP induction, and LPS-induced TNF-? production in the liver. Downregulation of STAT3 by siRNA attenuated the effect of nicotine on TTP expression and TNF-? production but did not affect the nicotine-mediated induction of HO-1. In TTP knockout mice, nicotine treatment enhanced HO-1 expression and STAT3 activation but failed to inhibit LPS-induced TNF-? production. Our results suggest that HO-1 and TTP are functionally linked in mediating the anti-inflammatory effects of nicotine; HO-1 is necessary for the induction of TTP by nicotine. This novel nicotine-HO-1-TTP signaling pathway provides new possibilities for the treatment of inflammatory diseases. Twit Text FOAVip A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine ????Free Radic Biol Med http://www.kidney.de/pget.php?&tw=1&pmid=24095726 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24095726 #FOAvip English Wikipedia <ref>{{Cite pmid|24095726 }}</ref> A functional link between heme oxygenase-1 and tristetraprolin in the anti-inflammatory effects of nicotine #MMPMID24095726 Jamal Uddin M ; Joe Y ; Zheng M ; Blackshear PJ ; Ryter SW ; Park JW ; Chung HT Free Radic Biol Med 2013[Dec]; 65 (ä): 1331-9 PMID24095726 show ga Nicotine stimulates the cholinergic anti-inflammatory pathway and prevents excessive inflammation by inhibiting the release of inflammatory cytokines from macrophages. We have previously reported that heme oxygenase-1 (HO-1) and tristetraprolin (TTP) are induced by nicotine and mediate the anti-inflammatory function of nicotine in macrophages. However, it was not clear whether the two molecules are functionally linked. In this study, we sought to determine whether HO-1 associates with TTP to mediate the anti-inflammatory effects of nicotine. Inhibition of HO-1 activity or HO-1 expression attenuated the effects of nicotine on STAT3 activation, TTP induction, and TNF-? production in LPS-treated macrophages. Induction of HO-1 expression increased the level of TTP in the absence of nicotine. In an LPS-induced endotoxemia model, HO-1 deficiency blocked the effects of nicotine on the STAT3 phosphorylation, TTP induction, and LPS-induced TNF-? production in the liver. Downregulation of STAT3 by siRNA attenuated the effect of nicotine on TTP expression and TNF-? production but did not affect the nicotine-mediated induction of HO-1. In TTP knockout mice, nicotine treatment enhanced HO-1 expression and STAT3 activation but failed to inhibit LPS-induced TNF-? production. Our results suggest that HO-1 and TTP are functionally linked in mediating the anti-inflammatory effects of nicotine; HO-1 is necessary for the induction of TTP by nicotine. This novel nicotine-HO-1-TTP signaling pathway provides new possibilities for the treatment of inflammatory diseases. |Animals [MESH] |Anti-Inflammatory Agents/adverse effects/immunology/pharmacology [MESH] |Cell Line [MESH] |Cell Proliferation/drug effects [MESH] |Cytokines/immunology/metabolism [MESH] |Endotoxemia/immunology [MESH] |Heme Oxygenase-1/antagonists & inhibitors/genetics/*immunology [MESH] |Inflammation/*drug therapy/immunology [MESH] |Lipopolysaccharides [MESH] |Liver/metabolism [MESH] |Macrophages/immunology [MESH] |Mice [MESH] |Mice, Inbred BALB C [MESH] |Mice, Knockout [MESH] |Nicotine/adverse effects/immunology/*pharmacology [MESH] |Phosphorylation/drug effects [MESH] |RNA Interference [MESH] |RNA, Small Interfering [MESH] |STAT3 Transcription Factor/genetics/*immunology [MESH] |Signal Transduction/drug effects/immunology [MESH] |Tristetraprolin/genetics/*immunology [MESH]A functional link between heme oxygenase-1 and tristetraprolin in the (epmc).pdf DeepDyve Pubget Overpricing