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10.1155/2017/2860956 http://scihub22266oqcxt.onion/10.1155/2017/2860956 C5350318!5350318!28348460     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28348460.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Mediators+Inflamm 2017 ; 2017 (�): � Nephropedia Template TP {{tp|p=28348460|t=2017. Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1? in Retinal Endothelial Cells and Mouse Retinal Vasculature |pdf=|usr=}}{{28348460}} gab.com Text Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1 in Retinal Endothelial Cells and Mouse Retinal Vasculature JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=28348460 #FOAvip Inflammation is an important component of diabetic retinal damage. We previously reported that a novel ?-adrenergic receptor agonist, Compound 49b, reduced Toll-like receptor 4 (TLR4) signaling in retinal endothelial cells (REC) grown in high glucose. Others reported that TLR4 activates high-mobility group box 1 (HMGB1), which has been associated with the NOD-like receptor 3 (NLRP3) inflammasome. Thus, we hypothesized that Epac1, a downstream mediator of ?-adrenergic receptors, would block TLR4/HMGB1-mediated stimulation of the NLRP3 inflammasome, leading to reduced cleavage of caspase-1 and interleukin-1 beta (IL-1?). We generated vascular specific conditional knockout mice for Epac1 and used REC grown in normal and high glucose treated with an Epac1 agonist and/or NLRP3 siRNA. Protein analyses were done for Epac1, TLR4, HMGB1, NLRP3, cleaved caspase-1, and IL-1?. Loss of Epac1 in the mouse retinal vasculature significantly increased all of the inflammatory proteins. Epac1 effectively reduced high glucose-induced increases in TLR4, HMGB1, cleaved caspase-1, and IL-1? in REC. Taken together, the data suggest that Epac1 reduces formation of the NLRP3 inflammasome to reduce inflammatory responses in the retinal vasculature. Twit Text FOAVip Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1 in Retinal Endothelial Cells and Mouse Retinal Vasculature ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=28348460 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28348460 #FOAvip English Wikipedia <ref>{{Cite pmid|28348460}}</ref> Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1? in Retinal Endothelial Cells and Mouse Retinal Vasculature #MMPMID28348460 Jiang Y; Liu L; Curtiss E; Steinle JJ Mediators Inflamm 2017[]; 2017 (�): � PMID28348460show ga Inflammation is an important component of diabetic retinal damage. We previously reported that a novel ?-adrenergic receptor agonist, Compound 49b, reduced Toll-like receptor 4 (TLR4) signaling in retinal endothelial cells (REC) grown in high glucose. Others reported that TLR4 activates high-mobility group box 1 (HMGB1), which has been associated with the NOD-like receptor 3 (NLRP3) inflammasome. Thus, we hypothesized that Epac1, a downstream mediator of ?-adrenergic receptors, would block TLR4/HMGB1-mediated stimulation of the NLRP3 inflammasome, leading to reduced cleavage of caspase-1 and interleukin-1 beta (IL-1?). We generated vascular specific conditional knockout mice for Epac1 and used REC grown in normal and high glucose treated with an Epac1 agonist and/or NLRP3 siRNA. Protein analyses were done for Epac1, TLR4, HMGB1, NLRP3, cleaved caspase-1, and IL-1?. Loss of Epac1 in the mouse retinal vasculature significantly increased all of the inflammatory proteins. Epac1 effectively reduced high glucose-induced increases in TLR4, HMGB1, cleaved caspase-1, and IL-1? in REC. Taken together, the data suggest that Epac1 reduces formation of the NLRP3 inflammasome to reduce inflammatory responses in the retinal vasculature. �Epac1 Blocks NLRP3 Inflammasome to Reduce IL-1? in Retinal Endothelial(epmc).pdf DeepDyve Pubget Overpricing