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10.1155/2015/506041 http://scihub22266oqcxt.onion/10.1155/2015/506041 C4436472!4436472!26074680     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 Deprecated: Implicit conversion from float 233.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Mediators+Inflamm 2015 ; 2015 (ä): ä Nephropedia Template TP {{tp|p=26074680|t=2015. TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2 |pdf=|usr=}}{{26074680}} gab.com Text TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2 JO: Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26074680 #FOAvip The CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF-? is considered the main fibrogenic cytokine; however, in some pathological settings TGF-? also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-?, but data on TGF-? role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF-? blockade in CCN2-mediated experimental renal damage. Systemic administration of the C-terminal module of CCN2 to mice caused sustained renal inflammation. In these mice, TGF-? blockade, using an anti-TGF-? neutralizing antibody, significantly increased renal expression of the NGAL (a kidney injury biomarker), kidney infiltration by monocytes/macrophages, and upregulation of MCP-1 expression. The anti-inflammatory effect of TGF-? seems to be mediated by a dysregulation of the systemic Treg immune response, shown by decreased levels of circulating CD4+/Foxp3+Treg cells. Our experimental data support the idea that TGF-? exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic target. Twit Text FOAVip TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2 ????Mediators Inflamm http://www.kidney.de/pget.php?&tw=1&pmid=26074680 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26074680 #FOAvip English Wikipedia <ref>{{Cite pmid|26074680}}</ref> TGF-Beta Blockade Increases Renal Inflammation Caused by the C-Terminal Module of the CCN2 #MMPMID26074680 Rodrigues-Díez R; Rayego-Mateos S; Orejudo M; Aroeira LS; Selgas R; Ortiz A; Egido J; Ruiz-Ortega M Mediators Inflamm 2015[]; 2015 (ä): ä PMID26074680show ga The CCN family member 2 (CCN2, also known as connective tissue growth factor) may behave as a risk biomarker and a potential therapeutic target for renal disease. CCN2 participates in the regulation of inflammation and fibrosis. TGF-? is considered the main fibrogenic cytokine; however, in some pathological settings TGF-? also has anti-inflammatory properties. CCN2 has been proposed as a downstream profibrotic mediator of TGF-?, but data on TGF-? role in CCN2 actions are scarce. Our aim was to evaluate the effect of TGF-? blockade in CCN2-mediated experimental renal damage. Systemic administration of the C-terminal module of CCN2 to mice caused sustained renal inflammation. In these mice, TGF-? blockade, using an anti-TGF-? neutralizing antibody, significantly increased renal expression of the NGAL (a kidney injury biomarker), kidney infiltration by monocytes/macrophages, and upregulation of MCP-1 expression. The anti-inflammatory effect of TGF-? seems to be mediated by a dysregulation of the systemic Treg immune response, shown by decreased levels of circulating CD4+/Foxp3+Treg cells. Our experimental data support the idea that TGF-? exerts anti-inflammatory actions in the kidney and suggest that it is not an optimal therapeutic target. äTGF-Beta Blockade Increases Renal Inflammation Caused by the C-Termina(epmc).pdf DeepDyve Pubget Overpricing