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10.1038/cddis.2017.74 http://scihub22266oqcxt.onion/10.1038/cddis.2017.74 C5386567!5386567!28277542     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 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 251.2 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Cell+Death+Dis 2017 ; 8 (3): e2658- Nephropedia Template TP {{tp|p=28277542|t=2017. MicroRNA-27a promotes podocyte injury via PPAR?-mediated ?-catenin activation in diabetic nephropathy |pdf=|usr=}}{{28277542}} gab.com Text MicroRNA-27a promotes podocyte injury via PPAR -mediated -catenin activation in diabetic nephropathy JO: Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28277542 #FOAvip Podocyte injury has a pivotal role in the pathogenesis of diabetic nephropathy (DN). MicroRNA-27a (miR-27a), peroxisome proliferator-activated receptor ? (PPAR?) and ?-catenin pathways have been involved in the pathogenesis of DN. Herein, we asked whether miR-27a mediates podocyte injury through PPAR?/?-catenin signaling in DN. The functional relevance of miR-27a, PPAR? and ?-catenin were investigated in cultured podocytes and glomeruli of diabetic rats and patients using in vitro and in vivo approaches. Podocyte injury was assessed by migration, invasion and apoptosis assay. Biological parameters were analyzed using enzyme-linked immunosorbent assay. We found that high glucose stimulated miR-27a expression, which, by negatively targeting PPAR?, activated ?-catenin signaling as evidenced by upregulation of ?-catenin target genes, snail1 and ?-smooth muscle actin (?-SMA) and downregulation of podocyte-specific markers podocin and synaptopodin. These changes caused podocyte injury as demonstrated by increased podocyte mesenchymal transition, disrupted podocyte architectural integrity and increased podocyte apoptosis. Furthermore, we provide evidence that miR-27a contributed to unfavorable renal function and increased podocyte injury in diabetic rats. Notably, miR-27a exhibited clinical and biological relevance as it was linked to elevated serum creatinine, proteinuria and reduced creatinine clearance rate. In addition, miR-27a upregulation and activation of PPAR?/?-catenin signaling were verified in renal biopsy samples from DN patients. We propose a novel role of the miR-27a/PPAR?/?-catenin axis in fostering the progression toward more deteriorated podocyte injury in DN. Targeting miR-27a could be a potential therapeutic approach for DN. Twit Text FOAVip MicroRNA-27a promotes podocyte injury via PPAR -mediated -catenin activation in diabetic nephropathy ????Cell Death Dis http://www.kidney.de/pget.php?&tw=1&pmid=28277542 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28277542 #FOAvip English Wikipedia <ref>{{Cite pmid|28277542}}</ref> MicroRNA-27a promotes podocyte injury via PPAR?-mediated ?-catenin activation in diabetic nephropathy #MMPMID28277542 Zhou Z; Wan J; Hou X; Geng J; Li X; Bai X Cell Death Dis 2017[Mar]; 8 (3): e2658- PMID28277542show ga Podocyte injury has a pivotal role in the pathogenesis of diabetic nephropathy (DN). MicroRNA-27a (miR-27a), peroxisome proliferator-activated receptor ? (PPAR?) and ?-catenin pathways have been involved in the pathogenesis of DN. Herein, we asked whether miR-27a mediates podocyte injury through PPAR?/?-catenin signaling in DN. The functional relevance of miR-27a, PPAR? and ?-catenin were investigated in cultured podocytes and glomeruli of diabetic rats and patients using in vitro and in vivo approaches. Podocyte injury was assessed by migration, invasion and apoptosis assay. Biological parameters were analyzed using enzyme-linked immunosorbent assay. We found that high glucose stimulated miR-27a expression, which, by negatively targeting PPAR?, activated ?-catenin signaling as evidenced by upregulation of ?-catenin target genes, snail1 and ?-smooth muscle actin (?-SMA) and downregulation of podocyte-specific markers podocin and synaptopodin. These changes caused podocyte injury as demonstrated by increased podocyte mesenchymal transition, disrupted podocyte architectural integrity and increased podocyte apoptosis. Furthermore, we provide evidence that miR-27a contributed to unfavorable renal function and increased podocyte injury in diabetic rats. Notably, miR-27a exhibited clinical and biological relevance as it was linked to elevated serum creatinine, proteinuria and reduced creatinine clearance rate. In addition, miR-27a upregulation and activation of PPAR?/?-catenin signaling were verified in renal biopsy samples from DN patients. We propose a novel role of the miR-27a/PPAR?/?-catenin axis in fostering the progression toward more deteriorated podocyte injury in DN. Targeting miR-27a could be a potential therapeutic approach for DN. äMicroRNA-27a promotes podocyte injury via PPAR?-mediated ?-catenin act(epmc).pdf DeepDyve Pubget Overpricing