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10.3389/fimmu.2018.01589 http://scihub22266oqcxt.onion/10.3389/fimmu.2018.01589 C6054981!6054981!30061884     free     free     free Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Front+Immunol 2018 ; 9 (ä): ä Nephropedia Template TP {{tp|p=30061884|t=2018. P2Y2R Signaling Is Involved in the Onset of Glomerulonephritis |pdf=|usr=}}{{30061884}} gab.com Text P2Y2R Signaling Is Involved in the Onset of Glomerulonephritis JO: Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=30061884 #FOAvip Endogenously released adenosine-5?-triphosphate (ATP) is a key regulator of physiological function and inflammatory responses in the kidney. Genetic or pharmacological inhibition of purinergic receptors has been linked to attenuation of inflammatory disorders and hence constitutes promising new avenues for halting and reverting inflammatory renal diseases. However, the involvement of purinergic receptors in glomerulonephritis (GN) has only been incompletely mapped. Here, we demonstrate that induction of GN in an experimental antibody-mediated GN model results in a significant increase of urinary ATP-levels and an upregulation of P2Y2R expression in resident kidney cells as well as infiltrating leukocytes pointing toward a possible role of the ATP/P2Y2R-axis in glomerular disease initiation. In agreement, decreasing extracellular ATP-levels or inhibition of P2R during induction of antibody-mediated GN leads to a reduction in all cardinal features of GN such as proteinuria, glomerulosclerosis, and renal failure. The specific involvement of P2Y2R could be further substantiated by demonstrating the protective effect of the lack of P2Y2R in antibody-mediated GN. To systematically differentiate between the function of P2Y2R on resident renal cells versus infiltrating leukocytes, we performed bone marrow-chimera experiments revealing that P2Y2R on hematopoietic cells is the main driver of the ATP/P2Y2R-mediated disease progression in antibody-mediated GN. Thus, these data unravel an important pro-inflammatory role for P2Y2R in the pathogenesis of GN. Twit Text FOAVip P2Y2R Signaling Is Involved in the Onset of Glomerulonephritis ????Front Immunol http://www.kidney.de/pget.php?&tw=1&pmid=30061884 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=30061884 #FOAvip English Wikipedia <ref>{{Cite pmid|30061884}}</ref> P2Y2R Signaling Is Involved in the Onset of Glomerulonephritis #MMPMID30061884 Rennert L; Zschiedrich S; Sandner L; Hartleben B; Cicko S; Ayata CK; Meyer C; Zech A; Zeiser R; Huber TB; Idzko M; Grahammer F Front Immunol 2018[]; 9 (ä): ä PMID30061884show ga Endogenously released adenosine-5?-triphosphate (ATP) is a key regulator of physiological function and inflammatory responses in the kidney. Genetic or pharmacological inhibition of purinergic receptors has been linked to attenuation of inflammatory disorders and hence constitutes promising new avenues for halting and reverting inflammatory renal diseases. However, the involvement of purinergic receptors in glomerulonephritis (GN) has only been incompletely mapped. Here, we demonstrate that induction of GN in an experimental antibody-mediated GN model results in a significant increase of urinary ATP-levels and an upregulation of P2Y2R expression in resident kidney cells as well as infiltrating leukocytes pointing toward a possible role of the ATP/P2Y2R-axis in glomerular disease initiation. In agreement, decreasing extracellular ATP-levels or inhibition of P2R during induction of antibody-mediated GN leads to a reduction in all cardinal features of GN such as proteinuria, glomerulosclerosis, and renal failure. The specific involvement of P2Y2R could be further substantiated by demonstrating the protective effect of the lack of P2Y2R in antibody-mediated GN. To systematically differentiate between the function of P2Y2R on resident renal cells versus infiltrating leukocytes, we performed bone marrow-chimera experiments revealing that P2Y2R on hematopoietic cells is the main driver of the ATP/P2Y2R-mediated disease progression in antibody-mediated GN. Thus, these data unravel an important pro-inflammatory role for P2Y2R in the pathogenesis of GN. äP2Y2R Signaling Is Involved in the Onset of Glomerulonephritis (epmc).pdf DeepDyve Pubget Overpricing