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10.1091/mbc.E16-02-0126 http://scihub22266oqcxt.onion/10.1091/mbc.E16-02-0126 C5221624!5221624 !27807045     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27807045 &cmd=llinks): Failed to open stream: HTTP request failed! 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HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway |pdf=|usr=}}{{27807045 }} gab.com Text HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway JO: Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27807045 #FOAvip We performed studies to determine the role of high-mobility group box 1 (HMGB1) in cigarette smoke (CS)-induced pulmonary inflammation. After mice were exposed to five cigarettes four times a day for 3 d, toll-like receptor 4 (TLR4) expression and TLR4-mediated signaling were significantly up-regulated, and HMGB1 had translocated from the nucleus to the cytoplasm in lung epithelial cells and then been released into the extracellular lung space. On CS exposure, inflammatory cell recruitment and proinflammatory cytokine production were significantly increased in lung tissue and bronchoalveolar lavage, and these effects depended on the TLR4 signaling pathway. HMGB1 inhibition decreased the CS-induced inflammatory response, whereas treatment with exogenous HMGB1 aggravated the damage and increased the phosphorylation of JNK, p38, and I?B? in the lungs of wild-type mice but not in TLR4-knockout mice. Blockade of TLR4 action or TLR4 knockout significantly inhibited HMGB1-induced proinflammatory cytokine production in mouse tracheal epithelial (MTE) cells and lung tissues. In addition, a MyD88 deficiency inhibited JNK, p38, and I?B? phosphorylation, and this effect was associated with the suppressed production of TNF-? and IL-1? in MTE cells and lung tissues in response to CS stimulation. Thus HMGB1 activates the NF-?B and JNK/p38 pathways through TLR4/MyD88-dependent signaling and induces an inflammatory response in lungs exposed to CS. Twit Text FOAVip HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway ????Mol Biol Cell http://www.kidney.de/pget.php?&tw=1&pmid=27807045 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27807045 #FOAvip English Wikipedia <ref>{{Cite pmid|27807045 }}</ref> HMGB1 translocation and release mediate cigarette smoke-induced pulmonary inflammation in mice through a TLR4/MyD88-dependent signaling pathway #MMPMID27807045 Cheng Y ; Wang D ; Wang B ; Li H ; Xiong J ; Xu S ; Chen Q ; Tao K ; Yang X ; Zhu Y ; He S Mol Biol Cell 2017[Jan]; 28 (1 ): 201-209 PMID27807045 show ga We performed studies to determine the role of high-mobility group box 1 (HMGB1) in cigarette smoke (CS)-induced pulmonary inflammation. After mice were exposed to five cigarettes four times a day for 3 d, toll-like receptor 4 (TLR4) expression and TLR4-mediated signaling were significantly up-regulated, and HMGB1 had translocated from the nucleus to the cytoplasm in lung epithelial cells and then been released into the extracellular lung space. On CS exposure, inflammatory cell recruitment and proinflammatory cytokine production were significantly increased in lung tissue and bronchoalveolar lavage, and these effects depended on the TLR4 signaling pathway. HMGB1 inhibition decreased the CS-induced inflammatory response, whereas treatment with exogenous HMGB1 aggravated the damage and increased the phosphorylation of JNK, p38, and I?B? in the lungs of wild-type mice but not in TLR4-knockout mice. Blockade of TLR4 action or TLR4 knockout significantly inhibited HMGB1-induced proinflammatory cytokine production in mouse tracheal epithelial (MTE) cells and lung tissues. In addition, a MyD88 deficiency inhibited JNK, p38, and I?B? phosphorylation, and this effect was associated with the suppressed production of TNF-? and IL-1? in MTE cells and lung tissues in response to CS stimulation. Thus HMGB1 activates the NF-?B and JNK/p38 pathways through TLR4/MyD88-dependent signaling and induces an inflammatory response in lungs exposed to CS. |Animals [MESH] |Cytokines/metabolism [MESH] |HMGB1 Protein/*metabolism [MESH] |Interleukin-1beta/pharmacology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Knockout [MESH] |Myeloid Differentiation Factor 88/metabolism [MESH] |NF-kappa B/metabolism [MESH] |Pneumonia/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Smoking/metabolism/*pathology [MESH] |Toll-Like Receptor 4/metabolism [MESH]HMGB1 translocation and release mediate cigarette smoke-induced pulmon(epmc).pdf DeepDyve Pubget Overpricing