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10.1681/ASN.2016010060 http://scihub22266oqcxt.onion/10.1681/ASN.2016010060 C5407712!5407712 !27895155     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27895155 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\27895155 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       J+Am+Soc+Nephrol 2017 ; 28 (5 ): 1408-1420 Nephropedia Template TP {{tp|p=27895155 |t=2017. Investigations of Glucocorticoid Action in GN |pdf=|usr=}}{{27895155 }} gab.com Text Investigations of Glucocorticoid Action in GN JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27895155 #FOAvip For several decades, glucocorticoids have been used empirically to treat rapid progressive GN. It is commonly assumed that glucocorticoids act primarily by dampening the immune response, but the mechanisms remain incompletely understood. In this study, we inactivated the glucocorticoid receptor (GR) specifically in kidney epithelial cells using Pax8-Cre/GR(fl/fl) mice. Pax8-Cre/GR(fl/fl) mice did not exhibit an overt spontaneous phenotype. In mice treated with nephrotoxic serum to induce crescentic nephritis (rapidly progressive GN), this genetic inactivation of the GR in kidney epithelial cells exerted renal benefits, including inhibition of albuminuria and cellular crescent formation, similar to the renal benefits observed with high-dose prednisolone in control mice. However, genetic inactivation of the GR in kidney epithelial cells did not induce the immunosuppressive effects observed with prednisolone. In vitro, prednisolone and the pharmacologic GR antagonist mifepristone each acted directly on primary cultures of parietal epithelial cells, inhibiting cellular outgrowth and proliferation. In wild-type mice, pharmacologic treatment with the GR antagonist mifepristone also attenuated disease as effectively as high-dose prednisolone without the systemic immunosuppressive effects. Collectively, these data show that glucocorticoids act directly on activated glomerular parietal epithelial cells in crescentic nephritis. Furthermore, we identified a novel therapeutic approach in crescentic nephritis, that of glucocorticoid antagonism, which was at least as effective as high-dose prednisolone with potentially fewer adverse effects. Twit Text FOAVip Investigations of Glucocorticoid Action in GN ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=27895155 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27895155 #FOAvip English Wikipedia <ref>{{Cite pmid|27895155 }}</ref> Investigations of Glucocorticoid Action in GN #MMPMID27895155 Kuppe C ; van Roeyen C ; Leuchtle K ; Kabgani N ; Vogt M ; Van Zandvoort M ; Smeets B ; Floege J ; Gröne HJ ; Moeller MJ J Am Soc Nephrol 2017[May]; 28 (5 ): 1408-1420 PMID27895155 show ga For several decades, glucocorticoids have been used empirically to treat rapid progressive GN. It is commonly assumed that glucocorticoids act primarily by dampening the immune response, but the mechanisms remain incompletely understood. In this study, we inactivated the glucocorticoid receptor (GR) specifically in kidney epithelial cells using Pax8-Cre/GR(fl/fl) mice. Pax8-Cre/GR(fl/fl) mice did not exhibit an overt spontaneous phenotype. In mice treated with nephrotoxic serum to induce crescentic nephritis (rapidly progressive GN), this genetic inactivation of the GR in kidney epithelial cells exerted renal benefits, including inhibition of albuminuria and cellular crescent formation, similar to the renal benefits observed with high-dose prednisolone in control mice. However, genetic inactivation of the GR in kidney epithelial cells did not induce the immunosuppressive effects observed with prednisolone. In vitro, prednisolone and the pharmacologic GR antagonist mifepristone each acted directly on primary cultures of parietal epithelial cells, inhibiting cellular outgrowth and proliferation. In wild-type mice, pharmacologic treatment with the GR antagonist mifepristone also attenuated disease as effectively as high-dose prednisolone without the systemic immunosuppressive effects. Collectively, these data show that glucocorticoids act directly on activated glomerular parietal epithelial cells in crescentic nephritis. Furthermore, we identified a novel therapeutic approach in crescentic nephritis, that of glucocorticoid antagonism, which was at least as effective as high-dose prednisolone with potentially fewer adverse effects. |Animals [MESH] |Epithelium [MESH] |Glomerulonephritis/*drug therapy [MESH] |Glucocorticoids/*pharmacology/*therapeutic use [MESH] |Kidney Glomerulus/drug effects/physiopathology [MESH] |Mice [MESH] |Prednisolone [MESH]Investigations of Glucocorticoid Action in GN (epmc).pdf DeepDyve Pubget Overpricing