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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.

10.1111/acel.12563 http://scihub22266oqcxt.onion/10.1111/acel.12563 C5334541!5334541 !28127848     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 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 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 Deprecated: Implicit conversion from float 211.6 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\28127848 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Aging+Cell 2017 ; 16 (2 ): 387-400 Nephropedia Template TP {{tp|p=28127848 |t=2017. MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice |pdf=|usr=}}{{28127848 }} gab.com Text MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice JO: Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=28127848 #FOAvip Epithelial-to-mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR-30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the roles of miR-30c in EMT and tubulointerstitial fibrosis, recombinant adeno-associated viral vector was applied to manipulate the expression of miR-30c. In vivo study showed that overexpression of miR-30c suppressed EMT, attenuated renal tubulointerstitial fibrosis and reduced proteinuria, serum creatinine, and BUN levels. In addition, Snail1 was identified as a direct target of miR-30c by Ago2 co-immunoprecipitation, luciferase reporter, and Western blot assays. Downregulating Snail1 by siRNA reduced high glucose-induced EMT in HK2 cells, and miR-30c mimicked the effects. Moreover, miR-30c inhibited Snail1-TGF-?1 axis in tubular epithelial cells undergoing EMT and thereby impeded the release of TGF-?1; oppositely, knockdown of miR-30c enhanced the secretion of TGF-?1 from epitheliums and significantly promoted proliferation of fibroblasts and fibrogenesis of myofibroblasts, aggravated tubulointerstitial fibrosis, and dysfunction of diabetic nephropathy. These results suggest a protective role of miR-30c against diabetic nephropathy by suppressing EMT via inhibiting Snail1-TGF-?1 pathway. Twit Text FOAVip MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice ????Aging Cell http://www.kidney.de/pget.php?&tw=1&pmid=28127848 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28127848 #FOAvip English Wikipedia <ref>{{Cite pmid|28127848 }}</ref> MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mesenchymal transition in db/db mice #MMPMID28127848 Zhao Y ; Yin Z ; Li H ; Fan J ; Yang S ; Chen C ; Wang DW Aging Cell 2017[Apr]; 16 (2 ): 387-400 PMID28127848 show ga Epithelial-to-mesenchymal transition (EMT) plays a significant role in tubulointerstitial fibrosis, which is a hallmark of diabetic nephropathy. Thus, identifying the mechanisms of EMT activation could be meaningful. In this study, loss of miR-30c accompanied with increased EMT was observed in renal tubules of db/db mice and cultured HK2 cells exposed to high glucose. To further explore the roles of miR-30c in EMT and tubulointerstitial fibrosis, recombinant adeno-associated viral vector was applied to manipulate the expression of miR-30c. In vivo study showed that overexpression of miR-30c suppressed EMT, attenuated renal tubulointerstitial fibrosis and reduced proteinuria, serum creatinine, and BUN levels. In addition, Snail1 was identified as a direct target of miR-30c by Ago2 co-immunoprecipitation, luciferase reporter, and Western blot assays. Downregulating Snail1 by siRNA reduced high glucose-induced EMT in HK2 cells, and miR-30c mimicked the effects. Moreover, miR-30c inhibited Snail1-TGF-?1 axis in tubular epithelial cells undergoing EMT and thereby impeded the release of TGF-?1; oppositely, knockdown of miR-30c enhanced the secretion of TGF-?1 from epitheliums and significantly promoted proliferation of fibroblasts and fibrogenesis of myofibroblasts, aggravated tubulointerstitial fibrosis, and dysfunction of diabetic nephropathy. These results suggest a protective role of miR-30c against diabetic nephropathy by suppressing EMT via inhibiting Snail1-TGF-?1 pathway. |*Epithelial-Mesenchymal Transition/drug effects [MESH] |Animals [MESH] |Base Sequence [MESH] |Diabetic Nephropathies/*genetics/*pathology [MESH] |Down-Regulation/drug effects/*genetics [MESH] |Epithelial Cells/drug effects/metabolism [MESH] |Glucose/toxicity [MESH] |HEK293 Cells [MESH] |Humans [MESH] |Kidney Tubules/drug effects/pathology/physiopathology [MESH] |Mice, Inbred C57BL [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Protective Agents/*metabolism [MESH] |Snail Family Transcription Factors/metabolism [MESH]MiR-30c protects diabetic nephropathy by suppressing epithelial-to-mes(epmc).pdf DeepDyve Pubget Overpricing