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10.1038/srep37492 http://scihub22266oqcxt.onion/10.1038/srep37492 C5118685!5118685!27874055     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27874055&cmd=llinks): Failed to open stream: HTTP request failed! 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The coordinated roles of miR-26a and miR-30c in regulating TGF?1-induced epithelial-to-mesenchymal transition in diabetic nephropathy |pdf=|usr=}}{{27874055}} gab.com Text The coordinated roles of miR-26a and miR-30c in regulating TGF 1-induced epithelial-to-mesenchymal transition in diabetic nephropathy JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27874055 #FOAvip MicroRNAs (miRNAs) play vital roles in the development of diabetic nephropathy. Here, we compared the protective efficacies of miR-26a and miR-30c in renal tubular epithelial cells (NRK-52E) and determined whether they demonstrated additive effects in the attenuation of renal fibrosis. TGF?1 suppressed miR-26a and miR-30c expression but up-regulated pro-fibrotic markers in NRK-52E cells, and these changes were also found in the kidney cortex of 40-week-old diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats. Bioinformatic analyses and luciferase assays further demonstrated that both miR-26a and miR-30c targeted connective tissue growth factor (CTGF); additionally, Snail family zinc finger 1 (Snail1), a potent epithelial-to-mesenchymal transition (EMT) inducer, was targeted by miR-30c. Overexpression of miR-26a and miR-30c coordinately decreased CTGF protein levels and subsequently ameliorated TGF?1-induced EMT in NRK-52E cells. Co-silencing of miR-26a and miR-30c exhibited the opposite effect. Moreover, miR-26a and miR-30c co-silenced CTGF to decrease ERK1/2 and p38 MAPK activation. Furthermore, miR-26a was up-regulated in urinary extracellular vesicles of diabetic nephropathy patients. Our study provides evidence for the cooperative roles of miR-26a and miR-30c in the pathogenesis of diabetic nephropathy, and the co-targeting of miR-26a and miR-30c could provide a new direction for diabetic nephropathy treatment. Twit Text FOAVip The coordinated roles of miR-26a and miR-30c in regulating TGF 1-induced epithelial-to-mesenchymal transition in diabetic nephropathy ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=27874055 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27874055 #FOAvip English Wikipedia <ref>{{Cite pmid|27874055}}</ref> The coordinated roles of miR-26a and miR-30c in regulating TGF?1-induced epithelial-to-mesenchymal transition in diabetic nephropathy #MMPMID27874055 Zheng Z; Guan M; Jia Y; Wang D; Pang R; Lv F; Xiao Z; Wang L; Zhang H; Xue Y Sci Rep 2016[]; 6 (ä): ä PMID27874055show ga MicroRNAs (miRNAs) play vital roles in the development of diabetic nephropathy. Here, we compared the protective efficacies of miR-26a and miR-30c in renal tubular epithelial cells (NRK-52E) and determined whether they demonstrated additive effects in the attenuation of renal fibrosis. TGF?1 suppressed miR-26a and miR-30c expression but up-regulated pro-fibrotic markers in NRK-52E cells, and these changes were also found in the kidney cortex of 40-week-old diabetic Otsuka Long-Evans Tokushima fatty (OLETF) rats. Bioinformatic analyses and luciferase assays further demonstrated that both miR-26a and miR-30c targeted connective tissue growth factor (CTGF); additionally, Snail family zinc finger 1 (Snail1), a potent epithelial-to-mesenchymal transition (EMT) inducer, was targeted by miR-30c. Overexpression of miR-26a and miR-30c coordinately decreased CTGF protein levels and subsequently ameliorated TGF?1-induced EMT in NRK-52E cells. Co-silencing of miR-26a and miR-30c exhibited the opposite effect. Moreover, miR-26a and miR-30c co-silenced CTGF to decrease ERK1/2 and p38 MAPK activation. Furthermore, miR-26a was up-regulated in urinary extracellular vesicles of diabetic nephropathy patients. Our study provides evidence for the cooperative roles of miR-26a and miR-30c in the pathogenesis of diabetic nephropathy, and the co-targeting of miR-26a and miR-30c could provide a new direction for diabetic nephropathy treatment. äThe coordinated roles of miR-26a and miR-30c in regulating TGF?1-induc(epmc).pdf DeepDyve Pubget Overpricing