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10.1161/CIRCRESAHA.116.305406 http://scihub22266oqcxt.onion/10.1161/CIRCRESAHA.116.305406 C4426092!4426092!25801896     free     free     free Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\25801896.jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Circ+Res 2015 ; 116 (10): 1670-9 Nephropedia Template TP {{tp|p=25801896|t=2015. Haptoglobin Enhances Cardiac Transplant Rejection |pdf=|usr=}}{{25801896}} gab.com Text Haptoglobin Enhances Cardiac Transplant Rejection JO: Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25801896 #FOAvip Rationale: Early graft inflammation enhances both acute and chronic rejection of heart transplants, but it is unclear how this inflammation is initiated. Objective: To identify specific inflammatory modulators and determine their underlying molecular mechanisms after cardiac transplantation. Methods and Results: We used a murine heterotopic cardiac transplant model to identify inflammatory modulators of early graft inflammation. Unbiased mass spectrometric analysis of cardiac tissue before and up to 72 hours after transplantation revealed that 22 proteins including haptoglobin, a known anti-oxidant, are significantly upregulated in our grafts. Through the use of haptoglobin deficient mice, we show that 80% of haptoglobin deficient recipients treated with peri-operative administration of the costimulatory blocking agent CTLA4 immunoglobulin exhibited > 100 days survival of full major histocompatibility complex mismatched allografts, whereas all similarly treated wild type recipients rejected their transplants by 21 days post transplantation. We found that haptoglobin modifies the intra-allograft inflammatory milieu by enhancing levels of the inflammatory cytokine IL-6 and the chemokine MIP-2 but impair levels of the immunosuppressive cytokine IL-10. Haptoglobin also enhances dendritic cell graft recruitment and augments anti-donor T cell responses. Moreover, we confirmed that the protein is present in human cardiac allograft specimens undergoing acute graft rejection. Conclusions: Our findings provide new insights into the mechanisms of inflammation after cardiac transplantation and suggest that, in contrast to its prior reported anti-oxidant function in vascular inflammation, haptoglobin is an enhancer of inflammation after cardiac transplantation. Haptoglobin may also be a key component in other sterile inflammatory conditions. Twit Text FOAVip Haptoglobin Enhances Cardiac Transplant Rejection ????Circ Res http://www.kidney.de/pget.php?&tw=1&pmid=25801896 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25801896 #FOAvip English Wikipedia <ref>{{Cite pmid|25801896}}</ref> Haptoglobin Enhances Cardiac Transplant Rejection #MMPMID25801896 Shen H; Heuzey E; Mori D; Wong C; Colangelo C; Chung LM; Bruce C; Slizovskiy IB; Booth CJ; Kreisel D; Goldstein DR Circ Res 2015[May]; 116 (10): 1670-9 PMID25801896show ga Rationale: Early graft inflammation enhances both acute and chronic rejection of heart transplants, but it is unclear how this inflammation is initiated. Objective: To identify specific inflammatory modulators and determine their underlying molecular mechanisms after cardiac transplantation. Methods and Results: We used a murine heterotopic cardiac transplant model to identify inflammatory modulators of early graft inflammation. Unbiased mass spectrometric analysis of cardiac tissue before and up to 72 hours after transplantation revealed that 22 proteins including haptoglobin, a known anti-oxidant, are significantly upregulated in our grafts. Through the use of haptoglobin deficient mice, we show that 80% of haptoglobin deficient recipients treated with peri-operative administration of the costimulatory blocking agent CTLA4 immunoglobulin exhibited > 100 days survival of full major histocompatibility complex mismatched allografts, whereas all similarly treated wild type recipients rejected their transplants by 21 days post transplantation. We found that haptoglobin modifies the intra-allograft inflammatory milieu by enhancing levels of the inflammatory cytokine IL-6 and the chemokine MIP-2 but impair levels of the immunosuppressive cytokine IL-10. Haptoglobin also enhances dendritic cell graft recruitment and augments anti-donor T cell responses. Moreover, we confirmed that the protein is present in human cardiac allograft specimens undergoing acute graft rejection. Conclusions: Our findings provide new insights into the mechanisms of inflammation after cardiac transplantation and suggest that, in contrast to its prior reported anti-oxidant function in vascular inflammation, haptoglobin is an enhancer of inflammation after cardiac transplantation. Haptoglobin may also be a key component in other sterile inflammatory conditions. äHaptoglobin Enhances Cardiac Transplant Rejection (epmc).pdf DeepDyve Pubget Overpricing