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10.1371/journal.pone.0121419 http://scihub22266oqcxt.onion/10.1371/journal.pone.0121419 C4370445!4370445!25799465     free     free     free Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 227.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       PLoS+One 2015 ; 10 (3): ä Nephropedia Template TP {{tp|p=25799465|t=2015. Renal Intercalated Cells Sense and Mediate Inflammation via the P2Y14 Receptor |pdf=|usr=}}{{25799465}} gab.com Text Renal Intercalated Cells Sense and Mediate Inflammation via the P2Y14 Receptor JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799465 #FOAvip Uncontrolled inflammation is one of the leading causes of kidney failure. Pro-inflammatory responses can occur in the absence of infection, a process called sterile inflammation. Here we show that the purinergic receptor P2Y14 (GPR105) is specifically and highly expressed in collecting duct intercalated cells (ICs) and mediates sterile inflammation in the kidney. P2Y14 is activated by UDP-glucose, a damage-associated molecular pattern molecule (DAMP) released by injured cells. We found that UDP-glucose increases pro-inflammatory chemokine expression in ICs as well as MDCK-C11 cells, and UDP-glucose activates the MEK1/2-ERK1/2 pathway in MDCK-C11 cells. These effects were prevented following inhibition of P2Y14 with the small molecule PPTN. Tail vein injection of mice with UDP-glucose induced the recruitment of neutrophils to the renal medulla. This study identifies ICs as novel sensors, mediators and effectors of inflammation in the kidney via P2Y14. Twit Text FOAVip Renal Intercalated Cells Sense and Mediate Inflammation via the P2Y14 Receptor ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=25799465 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25799465 #FOAvip English Wikipedia <ref>{{Cite pmid|25799465}}</ref> Renal Intercalated Cells Sense and Mediate Inflammation via the P2Y14 Receptor #MMPMID25799465 Azroyan A; Cortez-Retamozo V; Bouley R; Liberman R; Ruan YC; Kiselev E; Jacobson KA; Pittet MJ; Brown D; Breton S PLoS One 2015[]; 10 (3): ä PMID25799465show ga Uncontrolled inflammation is one of the leading causes of kidney failure. Pro-inflammatory responses can occur in the absence of infection, a process called sterile inflammation. Here we show that the purinergic receptor P2Y14 (GPR105) is specifically and highly expressed in collecting duct intercalated cells (ICs) and mediates sterile inflammation in the kidney. P2Y14 is activated by UDP-glucose, a damage-associated molecular pattern molecule (DAMP) released by injured cells. We found that UDP-glucose increases pro-inflammatory chemokine expression in ICs as well as MDCK-C11 cells, and UDP-glucose activates the MEK1/2-ERK1/2 pathway in MDCK-C11 cells. These effects were prevented following inhibition of P2Y14 with the small molecule PPTN. Tail vein injection of mice with UDP-glucose induced the recruitment of neutrophils to the renal medulla. This study identifies ICs as novel sensors, mediators and effectors of inflammation in the kidney via P2Y14. äRenal Intercalated Cells Sense and Mediate Inflammation via the P2Y14 (epmc).pdf DeepDyve Pubget Overpricing