Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

A dictionary by aggregated review articles of nephrology, medicine and the life sciences Your one-stop-run pathway from word to the immediate pdf of peer-reviewed on-topic knowledge.

10.1371/journal.pone.0174471 http://scihub22266oqcxt.onion/10.1371/journal.pone.0174471 C5370123!5370123 !28350874     free     free     free Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Warning: imagejpeg(C:\Inetpub\vhosts\kidney.de\httpdocs\phplern\28350874 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       PLoS+One 2017 ; 12 (3 ): e0174471 Nephropedia Template TP {{tp|p=28350874 |t=2017. SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy |pdf=|usr=}}{{28350874 }} gab.com Text SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy JO: PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28350874 #FOAvip Progressive reduction of SnoN is associated with gradual elevation of TGF-?1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-?1 signaling, with potential therapeutic benefits against TGF- ?1 -induced renal fibrosis. To characterize SnoN for its role in renal fibrosis, we assessed SnoN expression patterns in response to high glucose stress, and evaluated the effects of upregulating SnoN on renal fibrosis. High glucose stress induced significantly elevated SnoN, TGF-?1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions. Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis. Alternatively, EMT was suppressed by dominantly expressed exogenous SnoN without interfering with TGF-?1. Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy. Twit Text FOAVip SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy ????PLoS One http://www.kidney.de/pget.php?&tw=1&pmid=28350874 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28350874 #FOAvip English Wikipedia <ref>{{Cite pmid|28350874 }}</ref> SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy #MMPMID28350874 Liu L ; Shi M ; Wang Y ; Zhang C ; Su B ; Xiao Y ; Guo B PLoS One 2017[]; 12 (3 ): e0174471 PMID28350874 show ga Progressive reduction of SnoN is associated with gradual elevation of TGF-?1 during diabetic nephropathy progression, suggesting SnoN to be a possible mediator of TGF-?1 signaling, with potential therapeutic benefits against TGF- ?1 -induced renal fibrosis. To characterize SnoN for its role in renal fibrosis, we assessed SnoN expression patterns in response to high glucose stress, and evaluated the effects of upregulating SnoN on renal fibrosis. High glucose stress induced significantly elevated SnoN, TGF-?1, and Arkadia transcription; however, significantly reduced SnoN protein levels were observed under these conditions. Upregulating the SnoN protein was achieved by Arkadia knockdown, which resulted in inhibited high glucose-induced epithelial-mesenchymal transition (EMT) in renal tubular cells, the onset phase of renal fibrosis. Alternatively, EMT was suppressed by dominantly expressed exogenous SnoN without interfering with TGF-?1. Overall, renal SnoN upregulation ameliorates renal fibrosis by relieving high glucose-induced EMT; these findings support a translational approach targeting SnoN for the treatment of diabetic nephropathy. |*Up-Regulation [MESH] |Animals [MESH] |Blotting, Western [MESH] |Cadherins/genetics/metabolism [MESH] |Cell Line [MESH] |Diabetes Mellitus, Experimental/genetics/metabolism [MESH] |Diabetic Nephropathies/genetics/*metabolism [MESH] |Epithelial Cells/drug effects/metabolism [MESH] |Epithelial-Mesenchymal Transition/drug effects/genetics [MESH] |Fibrosis/genetics/metabolism [MESH] |Glucose/metabolism/pharmacology [MESH] |Humans [MESH] |Kidney Tubules, Proximal/drug effects/metabolism [MESH] |Kidney/drug effects/*metabolism/pathology [MESH] |Male [MESH] |Nerve Tissue Proteins/genetics/*metabolism [MESH] |RNA Interference [MESH] |Rats, Sprague-Dawley [MESH] |Reverse Transcriptase Polymerase Chain Reaction [MESH] |Transcription Factors/genetics/*metabolism [MESH] |Transcriptional Activation/drug effects [MESH] |Transforming Growth Factor beta1/genetics/metabolism [MESH]SnoN upregulation ameliorates renal fibrosis in diabetic nephropathy (epmc).pdf DeepDyve Pubget Overpricing