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10.1681/ASN.2014111136 http://scihub22266oqcxt.onion/10.1681/ASN.2014111136 C4769194!4769194 !26334030     free     free     free Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 209.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 243.2 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\26334030 .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 2016 ; 27 (3 ): 745-65 Nephropedia Template TP {{tp|p=26334030 |t=2016. Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis |pdf=|usr=}}{{26334030 }} gab.com Text Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26334030 #FOAvip Diabetes is the leading cause of kidney failure, accounting for >45% of new cases of dialysis. Diabetic nephropathy is characterized by inflammation, fibrosis, and oxidant stress, pathologic features that are shared by many other chronic inflammatory diseases. The cytokine IL-17A was initially implicated as a mediator of chronic inflammatory diseases, but recent studies dispute these findings and suggest that IL-17A can favorably modulate inflammation. Here, we examined the role of IL-17A in diabetic nephropathy. We observed that IL-17A levels in plasma and urine were reduced in patients with advanced diabetic nephropathy. Type 1 diabetic mice that are genetically deficient in IL-17A developed more severe nephropathy, whereas administration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diabetes. Moreover, IL-17A administration effectively treated, prevented, and reversed established nephropathy in genetic models of diabetes. Protective effects were also observed after administration of IL-17F but not IL-17C or IL-17E. Notably, tubular epithelial cell-specific overexpression of IL-17A was sufficient to suppress diabetic nephropathy. Mechanistically, IL-17A administration suppressed phosphorylation of signal transducer and activator of transcription 3, a central mediator of fibrosis, upregulated anti-inflammatory microglia/macrophage WAP domain protein in an AMP-activated protein kinase-dependent manner and favorably modulated renal oxidative stress and AMP-activated protein kinase activation. Administration of recombinant microglia/macrophage WAP domain protein suppressed diabetes-induced albuminuria and enhanced M2 marker expression. These observations suggest that the beneficial effects of IL-17 are isoform-specific and identify low-dose IL-17A administration as a promising therapeutic approach in diabetic kidney disease. Twit Text FOAVip Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=26334030 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26334030 #FOAvip English Wikipedia <ref>{{Cite pmid|26334030 }}</ref> Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Metabolic Syndrome, and Associated Organ Fibrosis #MMPMID26334030 Mohamed R ; Jayakumar C ; Chen F ; Fulton D ; Stepp D ; Gansevoort RT ; Ramesh G J Am Soc Nephrol 2016[Mar]; 27 (3 ): 745-65 PMID26334030 show ga Diabetes is the leading cause of kidney failure, accounting for >45% of new cases of dialysis. Diabetic nephropathy is characterized by inflammation, fibrosis, and oxidant stress, pathologic features that are shared by many other chronic inflammatory diseases. The cytokine IL-17A was initially implicated as a mediator of chronic inflammatory diseases, but recent studies dispute these findings and suggest that IL-17A can favorably modulate inflammation. Here, we examined the role of IL-17A in diabetic nephropathy. We observed that IL-17A levels in plasma and urine were reduced in patients with advanced diabetic nephropathy. Type 1 diabetic mice that are genetically deficient in IL-17A developed more severe nephropathy, whereas administration of low-dose IL-17A prevented diabetic nephropathy in models of type 1 and type 2 diabetes. Moreover, IL-17A administration effectively treated, prevented, and reversed established nephropathy in genetic models of diabetes. Protective effects were also observed after administration of IL-17F but not IL-17C or IL-17E. Notably, tubular epithelial cell-specific overexpression of IL-17A was sufficient to suppress diabetic nephropathy. Mechanistically, IL-17A administration suppressed phosphorylation of signal transducer and activator of transcription 3, a central mediator of fibrosis, upregulated anti-inflammatory microglia/macrophage WAP domain protein in an AMP-activated protein kinase-dependent manner and favorably modulated renal oxidative stress and AMP-activated protein kinase activation. Administration of recombinant microglia/macrophage WAP domain protein suppressed diabetes-induced albuminuria and enhanced M2 marker expression. These observations suggest that the beneficial effects of IL-17 are isoform-specific and identify low-dose IL-17A administration as a promising therapeutic approach in diabetic kidney disease. |AMP-Activated Protein Kinases/metabolism [MESH] |Albuminuria/urine [MESH] |Animals [MESH] |Antirheumatic Agents [MESH] |Diabetes Mellitus, Experimental/chemically induced/complications [MESH] |Diabetes Mellitus, Type 1/complications/genetics [MESH] |Diabetes Mellitus, Type 2/complications/genetics [MESH] |Diabetic Nephropathies/etiology/*prevention & control [MESH] |Epithelial Cells/metabolism/pathology [MESH] |Fibrosis [MESH] |Glomerular Filtration Rate [MESH] |Humans [MESH] |Interleukin-17/*administration & dosage/genetics/metabolism [MESH] |Kidney Glomerulus/*pathology [MESH] |Kidney Tubules/cytology [MESH] |Macrophages/metabolism [MESH] |Male [MESH] |Metabolic Syndrome/*prevention & control [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Mice, Inbred DBA [MESH] |Mice, Knockout [MESH] |Microglia/metabolism [MESH] |Milk Proteins/metabolism [MESH] |Oxidative Stress/drug effects [MESH] |Phosphorylation/drug effects [MESH] |Podocytes/pathology [MESH] |Protein Isoforms/*administration & dosage/metabolism [MESH] |STAT3 Transcription Factor/metabolism [MESH] |Signal Transduction/drug effects [MESH] |Streptozocin [MESH]Low-Dose IL-17 Therapy Prevents and Reverses Diabetic Nephropathy, Met(epmc).pdf DeepDyve Pubget Overpricing