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10.1681/ASN.2014070673 http://scihub22266oqcxt.onion/10.1681/ASN.2014070673 25644111!4587690!25644111     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (10): 2399-413 Nephropedia Template TP {{tp|p=25644111|t=2015. Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN |pdf=|usr=}}{{25644111}} gab.com Text Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25644111 #FOAvip Severe GN involves local neutrophil extracellular trap (NET) formation. We hypothesized a local cytotoxic effect of NET-related histone release in necrotizing GN. In vitro, histones from calf thymus or histones released by neutrophils undergoing NETosis killed glomerular endothelial cells, podocytes, and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as antihistone IgG, activated protein C, or heparin prevented this effect. Histone toxicity on glomeruli ex vivo was Toll-like receptor 2/4 dependent, and lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti-glomerular basement membrane GN involved NET formation and vascular necrosis, whereas blocking NET formation by peptidylarginine inhibition or preemptive anti-histone IgG injection significantly reduced all aspects of GN (i.e., vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment or activation of glomerular leukocytes, and glomerular crescent formation). To evaluate histones as a therapeutic target, mice with established GN were treated with three different histone-neutralizing agents. Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogating severe GN, whereas combination therapy had no additive effects. Together, these results indicate that NET-related histone release during GN elicits cytotoxic and immunostimulatory effects. Furthermore, neutralizing extracellular histones is still therapeutic when initiated in established GN. Twit Text FOAVip Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25644111 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25644111 #FOAvip English Wikipedia <ref>{{Cite pmid|25644111}}</ref> Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vascular Necrosis in Severe GN #MMPMID25644111 Kumar SV; Kulkarni OP; Mulay SR; Darisipudi MN; Romoli S; Thomasova D; Scherbaum CR; Hohenstein B; Hugo C; Muller S; Liapis H; Anders HJ J Am Soc Nephrol 2015[Oct]; 26 (10): 2399-413 PMID25644111show ga Severe GN involves local neutrophil extracellular trap (NET) formation. We hypothesized a local cytotoxic effect of NET-related histone release in necrotizing GN. In vitro, histones from calf thymus or histones released by neutrophils undergoing NETosis killed glomerular endothelial cells, podocytes, and parietal epithelial cells in a dose-dependent manner. Histone-neutralizing agents such as antihistone IgG, activated protein C, or heparin prevented this effect. Histone toxicity on glomeruli ex vivo was Toll-like receptor 2/4 dependent, and lack of TLR2/4 attenuated histone-induced renal thrombotic microangiopathy and glomerular necrosis in mice. Anti-glomerular basement membrane GN involved NET formation and vascular necrosis, whereas blocking NET formation by peptidylarginine inhibition or preemptive anti-histone IgG injection significantly reduced all aspects of GN (i.e., vascular necrosis, podocyte loss, albuminuria, cytokine induction, recruitment or activation of glomerular leukocytes, and glomerular crescent formation). To evaluate histones as a therapeutic target, mice with established GN were treated with three different histone-neutralizing agents. Anti-histone IgG, recombinant activated protein C, and heparin were equally effective in abrogating severe GN, whereas combination therapy had no additive effects. Together, these results indicate that NET-related histone release during GN elicits cytotoxic and immunostimulatory effects. Furthermore, neutralizing extracellular histones is still therapeutic when initiated in established GN. |Animals[MESH] |Blood Vessels/*pathology[MESH] |Cattle[MESH] |Extracellular Traps/drug effects/*physiology[MESH] |Glomerulonephritis/*complications/drug therapy/etiology[MESH] |Histones/drug effects/*physiology[MESH] |Mice[MESH] |Necrosis/etiology[MESH]Neutrophil Extracellular Trap-Related Extracellular Histones Cause Vas(epmc).pdf DeepDyve Pubget Overpricing