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10.1371/journal.pone.0154874 http://scihub22266oqcxt.onion/10.1371/journal.pone.0154874 C4856290!4856290 !27144281     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27144281 &cmd=llinks): Failed to open stream: HTTP request failed! 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MAP3K19 Is a Novel Regulator of TGF-? Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis |pdf=|usr=}}{{27144281 }} gab.com Text MAP3K19 Is a Novel Regulator of TGF- Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27144281 #FOAvip Idiopathic pulmonary fibrosis (IPF) is a progressive, debilitating disease for which two medications, pirfenidone and nintedanib, have only recently been approved for treatment. The cytokine TGF-? has been shown to be a central mediator in the disease process. We investigated the role of a novel kinase, MAP3K19, upregulated in IPF tissue, in TGF-?-induced signal transduction and in bleomycin-induced pulmonary fibrosis. MAP3K19 has a very limited tissue expression, restricted primarily to the lungs and trachea. In pulmonary tissue, expression was predominantly localized to alveolar and interstitial macrophages, bronchial epithelial cells and type II pneumocytes of the epithelium. MAP3K19 was also found to be overexpressed in bronchoalveolar lavage macrophages from IPF patients compared to normal patients. Treatment of A549 or THP-1 cells with either MAP3K19 siRNA or a highly potent and specific inhibitor reduced phospho-Smad2 & 3 nuclear translocation following TGF-? stimulation. TGF-?-induced gene transcription was also strongly inhibited by both the MAP3K19 inhibitor and nintedanib, whereas pirfenidone had a much less pronounced effect. In combination, the MAP3K19 inhibitor appeared to act synergistically with either pirfenidone or nintedanib, at the level of target gene transcription or protein production. Finally, in an animal model of IPF, inhibition of MAP3K19 strongly attenuated bleomycin-induced pulmonary fibrosis when administered either prophylactically ortherapeutically. In summary, these results strongly suggest that inhibition of MAP3K19 may have a beneficial therapeutic effect in the treatment of IPF and represents a novel strategy to target this disease. Twit Text FOAVip MAP3K19 Is a Novel Regulator of TGF- Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=27144281 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27144281 #FOAvip English Wikipedia <ref>{{Cite pmid|27144281 }}</ref> MAP3K19 Is a Novel Regulator of TGF-? Signaling That Impacts Bleomycin-Induced Lung Injury and Pulmonary Fibrosis #MMPMID27144281 Boehme SA ; Franz-Bacon K ; DiTirro DN ; Ly TW ; Bacon KB PLoS One 2016[]; 11 (5 ): e0154874 PMID27144281 show ga Idiopathic pulmonary fibrosis (IPF) is a progressive, debilitating disease for which two medications, pirfenidone and nintedanib, have only recently been approved for treatment. The cytokine TGF-? has been shown to be a central mediator in the disease process. We investigated the role of a novel kinase, MAP3K19, upregulated in IPF tissue, in TGF-?-induced signal transduction and in bleomycin-induced pulmonary fibrosis. MAP3K19 has a very limited tissue expression, restricted primarily to the lungs and trachea. In pulmonary tissue, expression was predominantly localized to alveolar and interstitial macrophages, bronchial epithelial cells and type II pneumocytes of the epithelium. MAP3K19 was also found to be overexpressed in bronchoalveolar lavage macrophages from IPF patients compared to normal patients. Treatment of A549 or THP-1 cells with either MAP3K19 siRNA or a highly potent and specific inhibitor reduced phospho-Smad2 & 3 nuclear translocation following TGF-? stimulation. TGF-?-induced gene transcription was also strongly inhibited by both the MAP3K19 inhibitor and nintedanib, whereas pirfenidone had a much less pronounced effect. In combination, the MAP3K19 inhibitor appeared to act synergistically with either pirfenidone or nintedanib, at the level of target gene transcription or protein production. Finally, in an animal model of IPF, inhibition of MAP3K19 strongly attenuated bleomycin-induced pulmonary fibrosis when administered either prophylactically ortherapeutically. In summary, these results strongly suggest that inhibition of MAP3K19 may have a beneficial therapeutic effect in the treatment of IPF and represents a novel strategy to target this disease. |A549 Cells [MESH] |Animals [MESH] |Bleomycin/*pharmacology [MESH] |Bronchoalveolar Lavage/methods [MESH] |Cell Line, Tumor [MESH] |Disease Models, Animal [MESH] |Epithelial Cells/drug effects/metabolism [MESH] |Female [MESH] |HeLa Cells [MESH] |Humans [MESH] |Idiopathic Pulmonary Fibrosis/metabolism [MESH] |Indoles/pharmacology [MESH] |Lung Injury/*chemically induced/*metabolism [MESH] |Lung/drug effects/metabolism [MESH] |MAP Kinase Kinase Kinases/*metabolism [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Pulmonary Fibrosis/*chemically induced/*metabolism [MESH] |Pyridones/pharmacology [MESH] |Signal Transduction/drug effects/physiology [MESH] |Transforming Growth Factor beta/*metabolism [MESH]MAP3K19 Is a Novel Regulator of TGF-? Signaling That Impacts Bleomycin(epmc).pdf DeepDyve Pubget Overpricing