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10.1681/ASN.2014020192 http://scihub22266oqcxt.onion/10.1681/ASN.2014020192 C4413759!4413759!25185988     free     free     free Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 211.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       J+Am+Soc+Nephrol 2015 ; 26 (5): 1115-25 Nephropedia Template TP {{tp|p=25185988|t=2015. EGF Receptor Deletion in Podocytes Attenuates Diabetic Nephropathy |pdf=|usr=}}{{25185988}} gab.com Text EGF Receptor Deletion in Podocytes Attenuates Diabetic Nephropathy JO: J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25185988 #FOAvip The generation of reactive oxygen species (ROS), particularly superoxide, by damaged or dysfunctional mitochondria has been postulated to be an initiating event in the development of diabetes complications. The glomerulus is a primary site of diabetic injury, and podocyte injury is a classic hallmark of diabetic glomerular lesions. In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFRpodKO) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFRpodKO mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. Furthermore, EGFRpodKO diabetic mice had less TGF-?1 expression, Smad2/3 phosphorylation, and glomerular fibronectin deposition. Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFRpodKO diabetic mice. Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-?1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-?1, cleaved caspase 3, and Bcl2. These alterations were inhibited by treatment with mito-tempol or apocynin or by inhibiting EGFR expression or activity. Thus, results of our studies utilizing mice with podocyte-specific EGFR deletion demonstrate that EGFR activation has a major role in activating pathways that mediate podocyte injury and loss in diabetic nephropathy. Twit Text FOAVip EGF Receptor Deletion in Podocytes Attenuates Diabetic Nephropathy ????J Am Soc Nephrol http://www.kidney.de/pget.php?&tw=1&pmid=25185988 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25185988 #FOAvip English Wikipedia <ref>{{Cite pmid|25185988}}</ref> EGF Receptor Deletion in Podocytes Attenuates Diabetic Nephropathy #MMPMID25185988 Chen J; Chen JK; Harris RC J Am Soc Nephrol 2015[May]; 26 (5): 1115-25 PMID25185988show ga The generation of reactive oxygen species (ROS), particularly superoxide, by damaged or dysfunctional mitochondria has been postulated to be an initiating event in the development of diabetes complications. The glomerulus is a primary site of diabetic injury, and podocyte injury is a classic hallmark of diabetic glomerular lesions. In streptozotocin-induced type 1 diabetes, podocyte-specific EGF receptor (EGFR) knockout mice (EGFRpodKO) and their wild-type (WT) littermates had similar levels of hyperglycemia and polyuria, but EGFRpodKO mice had significantly less albuminuria and less podocyte loss compared with WT diabetic mice. Furthermore, EGFRpodKO diabetic mice had less TGF-?1 expression, Smad2/3 phosphorylation, and glomerular fibronectin deposition. Immunoblotting of isolated glomerular lysates revealed that the upregulation of cleaved caspase 3 and downregulation of Bcl2 in WT diabetic mice were attenuated in EGFRpodKO diabetic mice. Administration of the SOD mimetic mito-tempol or the NADPH oxidase inhibitor apocynin attenuated the upregulation of p-c-Src, p-EGFR, p-ERK1/2, p-Smad2/3, and TGF-?1 expression and prevented the alteration of cleaved caspase 3 and Bcl2 expression in glomeruli of WT diabetic mice. High-glucose treatment of cultured mouse podocytes induced similar alterations in the production of ROS; phosphorylation of c-Src, EGFR, and Smad2/3; and expression of TGF-?1, cleaved caspase 3, and Bcl2. These alterations were inhibited by treatment with mito-tempol or apocynin or by inhibiting EGFR expression or activity. Thus, results of our studies utilizing mice with podocyte-specific EGFR deletion demonstrate that EGFR activation has a major role in activating pathways that mediate podocyte injury and loss in diabetic nephropathy. äEGF Receptor Deletion in Podocytes Attenuates Diabetic Nephropathy (epmc).pdf DeepDyve Pubget Overpricing