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10.1111/ajt.12447 http://scihub22266oqcxt.onion/10.1111/ajt.12447 24103001!ä!24103001 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 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Transplant 2013 ; 13 (11): 2805-18 Nephropedia Template TP {{tp|p=24103001|t=2013. RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival |pdf=|usr=}}{{24103001}} gab.com Text RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival JO: Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24103001 #FOAvip Kidney transplant injury occurs with ischemia and alloimmunity. Members of the receptor interacting protein kinase family (RIPK1,3) are key regulators of "necroptosis," a newly recognized, regulated form of necrosis. Necroptosis and apoptosis death appear to be counterbalanced as caspase-8 inhibition can divert death from apoptosis to necrosis. Inhibition of necroptosis in donor organs to limit injury has not been studied in transplant models. In this study, necroptosis was triggered in caspase inhibited tubular epithelial cells (TEC) exposed to tumor necrosis factor alpha in vitro, while RIPK1 inhibition with necrostatin-1 or use of RIPK3(-/-) TEC, prevented necroptosis. In vivo, short hairpin RNA silencing of caspase-8 in donor B6 mouse kidneys increased necroptosis, enhanced high-mobility group box 1 release, reduced renal function and accelerated rejection when transplanted into BALB/c recipients. Using ethidium homodimer perfusion to assess necrosis in vivo, necrosis was abrogated in RIPK3(-/-) kidneys postischemia. Following transplantation, recipients receiving RIPK3(-/-) kidneys had longer survival (p = 0.002) and improved renal function (p = 0.03) when compared to controls. In summary, we show for the first time that RIPK3-mediated necroptosis in donor kidneys can promote inflammatory injury, and has a major impact on renal ischemia-reperfusion injury and transplant survival. We suggest inhibition of necroptosis in donor organs may similarly provide a major clinical benefit. Twit Text FOAVip RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival ????Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=24103001 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=24103001 #FOAvip English Wikipedia <ref>{{Cite pmid|24103001}}</ref> RIPK3-mediated necroptosis promotes donor kidney inflammatory injury and reduces allograft survival #MMPMID24103001 Lau A; Wang S; Jiang J; Haig A; Pavlosky A; Linkermann A; Zhang ZX; Jevnikar AM Am J Transplant 2013[Nov]; 13 (11): 2805-18 PMID24103001show ga Kidney transplant injury occurs with ischemia and alloimmunity. Members of the receptor interacting protein kinase family (RIPK1,3) are key regulators of "necroptosis," a newly recognized, regulated form of necrosis. Necroptosis and apoptosis death appear to be counterbalanced as caspase-8 inhibition can divert death from apoptosis to necrosis. Inhibition of necroptosis in donor organs to limit injury has not been studied in transplant models. In this study, necroptosis was triggered in caspase inhibited tubular epithelial cells (TEC) exposed to tumor necrosis factor alpha in vitro, while RIPK1 inhibition with necrostatin-1 or use of RIPK3(-/-) TEC, prevented necroptosis. In vivo, short hairpin RNA silencing of caspase-8 in donor B6 mouse kidneys increased necroptosis, enhanced high-mobility group box 1 release, reduced renal function and accelerated rejection when transplanted into BALB/c recipients. Using ethidium homodimer perfusion to assess necrosis in vivo, necrosis was abrogated in RIPK3(-/-) kidneys postischemia. Following transplantation, recipients receiving RIPK3(-/-) kidneys had longer survival (p = 0.002) and improved renal function (p = 0.03) when compared to controls. In summary, we show for the first time that RIPK3-mediated necroptosis in donor kidneys can promote inflammatory injury, and has a major impact on renal ischemia-reperfusion injury and transplant survival. We suggest inhibition of necroptosis in donor organs may similarly provide a major clinical benefit. |*Graft Survival[MESH] |*Necrosis[MESH] |Allografts[MESH] |Animals[MESH] |Apoptosis[MESH] |Blotting, Western[MESH] |Caspase 8/chemistry/genetics/metabolism[MESH] |Graft Rejection/*etiology/metabolism/pathology[MESH] |Immunoenzyme Techniques[MESH] |Inflammation/*etiology/metabolism/pathology[MESH] |Kidney Transplantation[MESH] |Kidney/injuries/metabolism/*pathology[MESH] |Mice[MESH] |Mice, Inbred BALB C[MESH] |Mice, Inbred C57BL[MESH] |Mice, Knockout[MESH] |RNA, Messenger/genetics[MESH] |RNA, Small Interfering/genetics[MESH] |Real-Time Polymerase Chain Reaction[MESH] |Receptor-Interacting Protein Serine-Threonine Kinases/*physiology[MESH] |Reperfusion Injury/genetics/metabolism/*pathology[MESH] |Reverse Transcriptase Polymerase Chain Reaction[MESH]RIPK3-mediated necroptosis promotes donor kidney inflammatory injury a(epmc).pdf DeepDyve Pubget Overpricing