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10.1111/j.1600-6143.2010.03257.x http://scihub22266oqcxt.onion/10.1111/j.1600-6143.2010.03257.x C5472986!5472986!20840479     free     free     free Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 225.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 259.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Am+J+Transplant 2010 ; 10 (12): 2586-95 Nephropedia Template TP {{tp|p=20840479|t=2010. Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury |pdf=|usr=}}{{20840479}} gab.com Text Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury JO: Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=20840479 #FOAvip The vascular ectonucleotidases CD39 [ENTPD1 (ec-tonucleoside triphosphate diphosphohydrolase-1), EC 3.6.1.5] and CD73 [EC 3.1.3.5] generate adenosine from extracellular nucleotides. CD39 activity is critical in determining the response to ischemia-reperfusion injury (IRI), and CD39 null mice exhibit heightened sensitivity to renal IRI. Adenosine has multiple mechanisms of action in the vasculature including direct endothelial protection, antiinflammatory and antithrombotic effects and is protective in several models of IRI. Mice transgenic for human CD39 (hCD39) have increased capacity to generate adenosine. We therefore hypothesized that hCD39 transgenic mice would be protected from renal IRI. The overexpression of hCD39 conferred protection in a model of warm renal IRI, with reduced histological injury, less apoptosis and preserved serum creatinine and urea levels. Benefit was abrogated by pretreatment with an adenosine A2A receptor antagonist. Adoptive transfer experiments showed that expression of hCD39 on either the vasculature or circulating cells mitigated IRI. Furthermore, hCD39 transgenic kidneys transplanted into syngeneic recipients after prolonged cold storage performed significantly better and exhibited less histological injury than wild-type control grafts. Thus, systemic or local strategies to promote adenosine generation and signaling may have beneficial effects on warm and cold renal IRI, with implications for therapeutic application in clinical renal transplantation. Twit Text FOAVip Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury ????Am J Transplant http://www.kidney.de/pget.php?&tw=1&pmid=20840479 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=20840479 #FOAvip English Wikipedia <ref>{{Cite pmid|20840479}}</ref> Transgenic Overexpression of CD39 Protects Against Renal Ischemia-Reperfusion and Transplant Vascular Injury #MMPMID20840479 Crikis S; Lu B; Murray-Segal LM; Selan C; Robson SC; d?Apice AJF; Nandurkar HH; Cowan PJ; Dwyer KM Am J Transplant 2010[Dec]; 10 (12): 2586-95 PMID20840479show ga The vascular ectonucleotidases CD39 [ENTPD1 (ec-tonucleoside triphosphate diphosphohydrolase-1), EC 3.6.1.5] and CD73 [EC 3.1.3.5] generate adenosine from extracellular nucleotides. CD39 activity is critical in determining the response to ischemia-reperfusion injury (IRI), and CD39 null mice exhibit heightened sensitivity to renal IRI. Adenosine has multiple mechanisms of action in the vasculature including direct endothelial protection, antiinflammatory and antithrombotic effects and is protective in several models of IRI. Mice transgenic for human CD39 (hCD39) have increased capacity to generate adenosine. We therefore hypothesized that hCD39 transgenic mice would be protected from renal IRI. The overexpression of hCD39 conferred protection in a model of warm renal IRI, with reduced histological injury, less apoptosis and preserved serum creatinine and urea levels. Benefit was abrogated by pretreatment with an adenosine A2A receptor antagonist. Adoptive transfer experiments showed that expression of hCD39 on either the vasculature or circulating cells mitigated IRI. Furthermore, hCD39 transgenic kidneys transplanted into syngeneic recipients after prolonged cold storage performed significantly better and exhibited less histological injury than wild-type control grafts. Thus, systemic or local strategies to promote adenosine generation and signaling may have beneficial effects on warm and cold renal IRI, with implications for therapeutic application in clinical renal transplantation. äTransgenic Overexpression of CD39 Protects Against Renal Ischemia-Repe(epmc).pdf DeepDyve Pubget Overpricing