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10.1186/s12860-016-0084-x http://scihub22266oqcxt.onion/10.1186/s12860-016-0084-x C4774182!4774182!26932661     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 245.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       BMC+Cell+Biol 2016 ; 17 (ä): ä Nephropedia Template TP {{tp|p=26932661|t=2016. IL-27 inhibits the TGF-?1-induced epithelial-mesenchymal transition in alveolar epithelial cells |pdf=|usr=}}{{26932661}} gab.com Text IL-27 inhibits the TGF- 1-induced epithelial-mesenchymal transition in alveolar epithelial cells JO: BMC Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26932661 #FOAvip Background: IL-27 is a multifunctional cytokine that has both pro-inflammatory and anti-inflammatory functions. Although IL-27 has been shown to potently inhibit lung fibrosis, the detailed mechanism of IL-27 in this process is poorly understood. Epithelial?mesenchymal transition (EMT) is one of the key mechanisms involved in pulmonary fibrosis. We assessed the effects of IL-27 on TGF-?1-induced EMT in alveolar epithelial cells. Methods: A549 cells (a human AEC cell line) were incubated with TGF-?1, IL-27, or both TGF-?1 and IL-27, and changes in E-cadherin, ?-catenin, vimentin and a-SMA levels were measured using real-time PCR, western blotting and fluorescence microscopy. The related proteins in the JAK/STAT and TGF-?/Smad signalling pathways were examined by western blot. Results: IL-27 increased the expression of epithelial phenotypic markers, including E-cadherin and ?-catenin, and inhibited mesenchymal phenotypic markers, including vimentin and a-SMA in A549 cells. Moreover, TGF-?1-induced EMT was attenuated by IL-27. Furthermore, we found that TGF-?1 activated the phosphorylation of JAK1, STAT1, STAT3, STAT5, Smad1, Smad3 and Smad5, and IL-27 partially inhibited these changes in this process. When cells were treated with the STAT3 specific inhibitor wp1006 and the Smad3 specific inhibitor SIS3, the inhibition of EMT by IL-27 was significantly strengthened. Conclusion: Our results suggest that IL-27 attenuates epithelial?mesenchymal transition in alveolar epithelial cells in the absence or presence of TGF-?1 through the JAK/STAT and TGF-?/Smad signalling pathways. Electronic supplementary material: The online version of this article (doi:10.1186/s12860-016-0084-x) contains supplementary material, which is available to authorized users. Twit Text FOAVip IL-27 inhibits the TGF- 1-induced epithelial-mesenchymal transition in alveolar epithelial cells ????BMC Cell Biol http://www.kidney.de/pget.php?&tw=1&pmid=26932661 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26932661 #FOAvip English Wikipedia <ref>{{Cite pmid|26932661}}</ref> IL-27 inhibits the TGF-?1-induced epithelial-mesenchymal transition in alveolar epithelial cells #MMPMID26932661 Dong Z; Tai W; Lei W; Wang Y; Li Z; Zhang T BMC Cell Biol 2016[]; 17 (ä): ä PMID26932661show ga Background: IL-27 is a multifunctional cytokine that has both pro-inflammatory and anti-inflammatory functions. Although IL-27 has been shown to potently inhibit lung fibrosis, the detailed mechanism of IL-27 in this process is poorly understood. Epithelial?mesenchymal transition (EMT) is one of the key mechanisms involved in pulmonary fibrosis. We assessed the effects of IL-27 on TGF-?1-induced EMT in alveolar epithelial cells. Methods: A549 cells (a human AEC cell line) were incubated with TGF-?1, IL-27, or both TGF-?1 and IL-27, and changes in E-cadherin, ?-catenin, vimentin and a-SMA levels were measured using real-time PCR, western blotting and fluorescence microscopy. The related proteins in the JAK/STAT and TGF-?/Smad signalling pathways were examined by western blot. Results: IL-27 increased the expression of epithelial phenotypic markers, including E-cadherin and ?-catenin, and inhibited mesenchymal phenotypic markers, including vimentin and a-SMA in A549 cells. Moreover, TGF-?1-induced EMT was attenuated by IL-27. Furthermore, we found that TGF-?1 activated the phosphorylation of JAK1, STAT1, STAT3, STAT5, Smad1, Smad3 and Smad5, and IL-27 partially inhibited these changes in this process. When cells were treated with the STAT3 specific inhibitor wp1006 and the Smad3 specific inhibitor SIS3, the inhibition of EMT by IL-27 was significantly strengthened. Conclusion: Our results suggest that IL-27 attenuates epithelial?mesenchymal transition in alveolar epithelial cells in the absence or presence of TGF-?1 through the JAK/STAT and TGF-?/Smad signalling pathways. Electronic supplementary material: The online version of this article (doi:10.1186/s12860-016-0084-x) contains supplementary material, which is available to authorized users. äIL-27 inhibits the TGF-?1-induced epithelial-mesenchymal transition in(epmc).pdf DeepDyve Pubget Overpricing