Use my Search Websuite to scan PubMed, PMCentral, Journal Hosts and Journal Archives, FullText. Kick-your-searchterm to multiple Engines kick-your-query now !>

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.

10.1152/ajprenal.00458.2014 http://scihub22266oqcxt.onion/10.1152/ajprenal.00458.2014 C4269695!4269695 !25354942     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=25354942 &cmd=llinks): Failed to open stream: HTTP request failed! HTTP/1.1 429 Too Many Requests in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 215 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 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 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 276.79999999999995 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534 Deprecated: Implicit conversion from float 276.79999999999995 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\25354942 .jpg): Failed to open stream: No such file or directory in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 117       Am+J+Physiol+Renal+Physiol 2014 ; 307 (12 ): F1390-403 Nephropedia Template TP {{tp|p=25354942 |t=2014. Repression of let-7 by transforming growth factor-?1-induced Lin28 upregulates collagen expression in glomerular mesangial cells under diabetic conditions |pdf=|usr=}}{{25354942 }} gab.com Text Repression of let-7 by transforming growth factor- 1-induced Lin28 upregulates collagen expression in glomerular mesangial cells under diabetic conditions JO: Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25354942 #FOAvip Accumulation of mesangial extracellular matrix (ECM) proteins such as collagen type 1-?2 (Col1a2) and collagen type 4-?1 (Col4a1) is a key feature of diabetic nephropathy (DN). Transforming growth factor (TGF)-?1 plays important roles in ECM accumulation in DN, and evidence shows a mediatory role for microRNAs. In the present study, we found that microRNA let-7 family members (let-7b/c/d/g/i) were downregulated in TGF-?-treated mouse mesangial cells (MMCs) along with upregulation of Col1a2 and Col4a1. Ectopic expression of let-7b in TGF-?-treated MMCs attenuated Col1a2 and Col4a1 upregulation. Conversely, let-7b inhibitors increased Col1a2 and Col4a1 levels. Cotransfection of MMCs with mouse Col1a2 or Col4a1 3'-untranslated region luciferase constructs and let-7b inhibitors increased luciferase activity. However, constructs with let-7 target site mutations were unresponsive to TGF-?. TGF-?-induced 3'-untranslated region activity was attenuated by let-7b mimics, suggesting that Col1a2 and Col4a1 are direct targets of let-7b. In addition, Lin28b, a negative regulator of let-7 biogenesis, was upregulated in TGF-?-treated MMCs. Luciferase assays showed that the Lin28b promoter containing the Smad-binding element (SBE) responded to TGF-?, which was abolished in constructs without SBE. Chromatin immunoprecipitation assays showed TGF-?-induced enrichment of Smad2/3 at the Lin28b promoter, together suggesting that Lin28b is transcriptionally induced by TGF-? through SBE. Furthermore, let-7b levels were decreased, whereas Lin28b, Col1a2, and Col4a1 levels were increased, in glomeruli of diabetic mice compared with nondiabetic control mice, demonstrating the in vivo relevance of this Lin28/let-7/collagen axis. These results identify Lin28 as a new TGF-? target gene and suggest a novel role for the Lin28/let-7 pathway in controlling TGF-?-induced collagen accumulation in DN. Twit Text FOAVip Repression of let-7 by transforming growth factor- 1-induced Lin28 upregulates collagen expression in glomerular mesangial cells under diabetic conditions ????Am J Physiol Renal Physiol http://www.kidney.de/pget.php?&tw=1&pmid=25354942 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=25354942 #FOAvip English Wikipedia <ref>{{Cite pmid|25354942 }}</ref> Repression of let-7 by transforming growth factor-?1-induced Lin28 upregulates collagen expression in glomerular mesangial cells under diabetic conditions #MMPMID25354942 Park JT ; Kato M ; Lanting L ; Castro N ; Nam BY ; Wang M ; Kang SW ; Natarajan R Am J Physiol Renal Physiol 2014[Dec]; 307 (12 ): F1390-403 PMID25354942 show ga Accumulation of mesangial extracellular matrix (ECM) proteins such as collagen type 1-?2 (Col1a2) and collagen type 4-?1 (Col4a1) is a key feature of diabetic nephropathy (DN). Transforming growth factor (TGF)-?1 plays important roles in ECM accumulation in DN, and evidence shows a mediatory role for microRNAs. In the present study, we found that microRNA let-7 family members (let-7b/c/d/g/i) were downregulated in TGF-?-treated mouse mesangial cells (MMCs) along with upregulation of Col1a2 and Col4a1. Ectopic expression of let-7b in TGF-?-treated MMCs attenuated Col1a2 and Col4a1 upregulation. Conversely, let-7b inhibitors increased Col1a2 and Col4a1 levels. Cotransfection of MMCs with mouse Col1a2 or Col4a1 3'-untranslated region luciferase constructs and let-7b inhibitors increased luciferase activity. However, constructs with let-7 target site mutations were unresponsive to TGF-?. TGF-?-induced 3'-untranslated region activity was attenuated by let-7b mimics, suggesting that Col1a2 and Col4a1 are direct targets of let-7b. In addition, Lin28b, a negative regulator of let-7 biogenesis, was upregulated in TGF-?-treated MMCs. Luciferase assays showed that the Lin28b promoter containing the Smad-binding element (SBE) responded to TGF-?, which was abolished in constructs without SBE. Chromatin immunoprecipitation assays showed TGF-?-induced enrichment of Smad2/3 at the Lin28b promoter, together suggesting that Lin28b is transcriptionally induced by TGF-? through SBE. Furthermore, let-7b levels were decreased, whereas Lin28b, Col1a2, and Col4a1 levels were increased, in glomeruli of diabetic mice compared with nondiabetic control mice, demonstrating the in vivo relevance of this Lin28/let-7/collagen axis. These results identify Lin28 as a new TGF-? target gene and suggest a novel role for the Lin28/let-7 pathway in controlling TGF-?-induced collagen accumulation in DN. |3' Untranslated Regions [MESH] |Animals [MESH] |Binding Sites [MESH] |Cells, Cultured [MESH] |Collagen Type I/*metabolism [MESH] |Collagen Type IV/*metabolism [MESH] |Diabetes Mellitus, Experimental/chemically induced/genetics/*metabolism/pathology [MESH] |Diabetes Mellitus, Type 2/genetics/*metabolism/pathology [MESH] |Diabetic Nephropathies/genetics/*metabolism/pathology [MESH] |Dose-Response Relationship, Drug [MESH] |Down-Regulation [MESH] |Fibrosis [MESH] |Humans [MESH] |Mesangial Cells/*drug effects/metabolism/pathology [MESH] |Mice, Inbred C57BL [MESH] |MicroRNAs/genetics/*metabolism [MESH] |Mutation [MESH] |RNA Interference [MESH] |RNA-Binding Proteins/genetics/*metabolism [MESH] |Recombinant Proteins/pharmacology [MESH] |Signal Transduction/drug effects [MESH] |Smad2 Protein/metabolism [MESH] |Smad3 Protein/metabolism [MESH] |Streptozocin [MESH] |Transcription, Genetic/drug effects [MESH] |Transfection [MESH] |Transforming Growth Factor beta1/*pharmacology [MESH]Repression of let-7 by transforming growth factor-?1-induced Lin28 upr(epmc).pdf DeepDyve Pubget Overpricing