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10.1038/s41598-017-08711-6 http://scihub22266oqcxt.onion/10.1038/s41598-017-08711-6 C5569053!5569053!28835626     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): ä Nephropedia Template TP {{tp|p=28835626|t=2017. Mitigation of sepsis-induced inflammatory responses and organ injury through targeting Wnt/?-catenin signaling |pdf=|usr=}}{{28835626}} gab.com Text Mitigation of sepsis-induced inflammatory responses and organ injury through targeting Wnt/ -catenin signaling JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28835626 #FOAvip The Wnt/?-catenin pathway has been involved in regulating inflammation in various infectious and inflammatory diseases. Sepsis is a life-threatening condition caused by dysregulated inflammatory response to infection with no effective therapy available. Recently elevated Wnt/?-catenin signaling has been detected in sepsis. However, its contribution to sepsis-associated inflammatory response remains to be explored. In this study, we show that inhibition of Wnt/?-catenin signaling reduces inflammation and mitigates sepsis-induced organ injury. Using in vitro LPS-stimulated RAW264.7 macrophages, we demonstrate that a small-molecule inhibitor of ?-catenin responsive transcription, iCRT3, significantly reduces the LPS-induced Wnt/?-catenin activity and also inhibits TNF-? production and I?B degradation in a dose-dependent manner. Intraperitoneal administration of iCRT3 to C57BL/6 mice, subjected to cecal ligation and puncture-induced sepsis, decreases the plasma levels of proinflammatory cytokines and organ injury markers in a dose-dependent manner. The histological integrity of the lungs is improved with iCRT3 treatment, along with reduced lung collagen deposition and apoptosis. In addition, iCRT3 treatment also decreases the expression of the cytokines, neutrophil chemoattractants, as well as the MPO activity in the lungs of septic mice. Based on these findings we conclude that targeting the Wnt/?-Catenin pathway may provide a potential therapeutic approach for treatment of sepsis. Twit Text FOAVip Mitigation of sepsis-induced inflammatory responses and organ injury through targeting Wnt/ -catenin signaling ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28835626 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28835626 #FOAvip English Wikipedia <ref>{{Cite pmid|28835626}}</ref> Mitigation of sepsis-induced inflammatory responses and organ injury through targeting Wnt/?-catenin signaling #MMPMID28835626 Sharma A; Yang WL; Ochani M; Wang P Sci Rep 2017[]; 7 (ä): ä PMID28835626show ga The Wnt/?-catenin pathway has been involved in regulating inflammation in various infectious and inflammatory diseases. Sepsis is a life-threatening condition caused by dysregulated inflammatory response to infection with no effective therapy available. Recently elevated Wnt/?-catenin signaling has been detected in sepsis. However, its contribution to sepsis-associated inflammatory response remains to be explored. In this study, we show that inhibition of Wnt/?-catenin signaling reduces inflammation and mitigates sepsis-induced organ injury. Using in vitro LPS-stimulated RAW264.7 macrophages, we demonstrate that a small-molecule inhibitor of ?-catenin responsive transcription, iCRT3, significantly reduces the LPS-induced Wnt/?-catenin activity and also inhibits TNF-? production and I?B degradation in a dose-dependent manner. Intraperitoneal administration of iCRT3 to C57BL/6 mice, subjected to cecal ligation and puncture-induced sepsis, decreases the plasma levels of proinflammatory cytokines and organ injury markers in a dose-dependent manner. The histological integrity of the lungs is improved with iCRT3 treatment, along with reduced lung collagen deposition and apoptosis. In addition, iCRT3 treatment also decreases the expression of the cytokines, neutrophil chemoattractants, as well as the MPO activity in the lungs of septic mice. Based on these findings we conclude that targeting the Wnt/?-Catenin pathway may provide a potential therapeutic approach for treatment of sepsis. äMitigation of sepsis-induced inflammatory responses and organ injury t(epmc).pdf DeepDyve Pubget Overpricing