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10.4049/jimmunol.0803565 http://scihub22266oqcxt.onion/10.4049/jimmunol.0803565 C4827346!4827346!19454727     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19454727&cmd=llinks): Failed to open stream: HTTP request failed! 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Poly(ADP-Ribose) Polymerase-1 Regulates the Progression of Autoimmune Nephritis in Males by Inducing Necrotic Cell Death and Modulating Inflammation1 |pdf=|usr=}}{{19454727}} gab.com Text Poly(ADP-Ribose) Polymerase-1 Regulates the Progression of Autoimmune Nephritis in Males by Inducing Necrotic Cell Death and Modulating Inflammation1 JO: J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=19454727 #FOAvip Necrotic lesions and necrotic cell death characterize severe autoimmune nephritides, and contribute to local inflammation and to progression of the disease. Poly(ADP-ribose) polymerase-1 (PARP-1), a DNA repair enzyme, is involved in the induction of necrosis and is a key player in the acute and chronic inflammation. Therefore, we hypothesized that PARP-1 controls the severity of nephritis by mediating the induction of necrosis in the kidney. We used lupus and anti-glomerular basement membrane models of nephritis to determine the effects of PARP-1 on the inflammatory response in the kidney. We show in this study that PARP-1 is indeed activated during the course of glomerulonephritis. We also show that the absence of PARP-1 or its pharmacological inhibition results in milder nephritis, with lower blood urea nitrogen levels, reduced necrotic lesions, and higher survival rates. The relevance of PARP-1 showed a strong male sex specificity, and treatment of male mice with 17?-estradiol prolonged their survival during the course of nephritis. PARP-1 also regulated TNF-? expression and up-regulation of adhesion molecules, further supporting a role of PARP-1 in the inflammatory process within the kidney. Our results demonstrate that PARP-1 activation and consequent necrotic cell death play an important role in the pathogenesis of male nephritis, and suggest that PARP-1 can be a novel therapeutic target in glomerulonephritis. The Journal of Immunology, 2009, 182: 7297?7306. Twit Text FOAVip Poly(ADP-Ribose) Polymerase-1 Regulates the Progression of Autoimmune Nephritis in Males by Inducing Necrotic Cell Death and Modulating Inflammation1 ????J Immunol http://www.kidney.de/pget.php?&tw=1&pmid=19454727 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=19454727 #FOAvip English Wikipedia <ref>{{Cite pmid|19454727}}</ref> Poly(ADP-Ribose) Polymerase-1 Regulates the Progression of Autoimmune Nephritis in Males by Inducing Necrotic Cell Death and Modulating Inflammation1 #MMPMID19454727 Jog NR; Dinnall JA; Gallucci S; Madaio MP; Caricchio R J Immunol 2009[Jun]; 182 (11): 7297-306 PMID19454727show ga Necrotic lesions and necrotic cell death characterize severe autoimmune nephritides, and contribute to local inflammation and to progression of the disease. Poly(ADP-ribose) polymerase-1 (PARP-1), a DNA repair enzyme, is involved in the induction of necrosis and is a key player in the acute and chronic inflammation. Therefore, we hypothesized that PARP-1 controls the severity of nephritis by mediating the induction of necrosis in the kidney. We used lupus and anti-glomerular basement membrane models of nephritis to determine the effects of PARP-1 on the inflammatory response in the kidney. We show in this study that PARP-1 is indeed activated during the course of glomerulonephritis. We also show that the absence of PARP-1 or its pharmacological inhibition results in milder nephritis, with lower blood urea nitrogen levels, reduced necrotic lesions, and higher survival rates. The relevance of PARP-1 showed a strong male sex specificity, and treatment of male mice with 17?-estradiol prolonged their survival during the course of nephritis. PARP-1 also regulated TNF-? expression and up-regulation of adhesion molecules, further supporting a role of PARP-1 in the inflammatory process within the kidney. Our results demonstrate that PARP-1 activation and consequent necrotic cell death play an important role in the pathogenesis of male nephritis, and suggest that PARP-1 can be a novel therapeutic target in glomerulonephritis. The Journal of Immunology, 2009, 182: 7297?7306. äPoly(ADP-Ribose) Polymerase-1 Regulates the Progression of Autoimmune (epmc).pdf DeepDyve Pubget Overpricing