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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.

10.1186/s12967-015-0710-y http://scihub22266oqcxt.onion/10.1186/s12967-015-0710-y C4640239!4640239 !26552447     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=26552447 &cmd=llinks): Failed to open stream: HTTP request failed! 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High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway |pdf=|usr=}}{{26552447 }} gab.com Text High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway JO: J Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26552447 #FOAvip OBJECTIVE: Diabetic nephropathy (DN) is a serious complication that commonly confronted by diabetic patients. A common theory for the pathogenesis of this renal dysfunction in diabetes is cell injury, inflammation as well as oxidative stress. In this content, the detailed molecular mechanism underlying high glucose induced renal tubular epithelial injury was elaborated. METHODS: An in vivo rat model of diabetes by injecting streptozotocin (STZ) and an in vitro high glucose incubated renal tubular epithelial cell (HK-2) model were used. Expression levels of Keap1, nuclear Nrf2 and p65 were determined by western blotting. Level of microR-29 (miR-29) was assessed using quantitative RT-PCR. Combination of p65 and miR-29 promotor was assessed using chromatin immunoprecipitation. Keap1 3'-UTR activity was detected using luciferase reporter gene assay. Cell viability was determined using MTT assay. RESULTS: In diabetic rat, miR-29 was downregulated and its expression is negatively correlated with both of serum creatinine and creatinine clearance. In high glucose incubated HK-2 cell, deacetylases activity of Sirt1 was attenuated that leads to decreased activity of nuclear factor kappa B (NF-?B). NF-?B was demonstrated to regulate miR-29 expression by directly binding to its promotor. The data of luciferase assay showed that miR-29 directly targets to Keap1 mRNA. While high glucose induced down regulation of miR-29 contributed to enhancement of Keap1 expression that finally reduced Nrf2 content by ubiquitinating Nrf2. Additionally, overexpression of miR-29 effectively relieved high glucose-reduced cell viability. CONCLUSION: High glucose induces renal tubular epithelial injury via Sirt1/NF-?B/microR-29/Keap1 signal pathway. Twit Text FOAVip High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway ????J Transl Med http://www.kidney.de/pget.php?&tw=1&pmid=26552447 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=26552447 #FOAvip English Wikipedia <ref>{{Cite pmid|26552447 }}</ref> High glucose induces renal tubular epithelial injury via Sirt1/NF-kappaB/microR-29/Keap1 signal pathway #MMPMID26552447 Zhou L ; Xu DY ; Sha WG ; Shen L ; Lu GY ; Yin X ; Wang MJ J Transl Med 2015[Nov]; 13 (ä): 352 PMID26552447 show ga OBJECTIVE: Diabetic nephropathy (DN) is a serious complication that commonly confronted by diabetic patients. A common theory for the pathogenesis of this renal dysfunction in diabetes is cell injury, inflammation as well as oxidative stress. In this content, the detailed molecular mechanism underlying high glucose induced renal tubular epithelial injury was elaborated. METHODS: An in vivo rat model of diabetes by injecting streptozotocin (STZ) and an in vitro high glucose incubated renal tubular epithelial cell (HK-2) model were used. Expression levels of Keap1, nuclear Nrf2 and p65 were determined by western blotting. Level of microR-29 (miR-29) was assessed using quantitative RT-PCR. Combination of p65 and miR-29 promotor was assessed using chromatin immunoprecipitation. Keap1 3'-UTR activity was detected using luciferase reporter gene assay. Cell viability was determined using MTT assay. RESULTS: In diabetic rat, miR-29 was downregulated and its expression is negatively correlated with both of serum creatinine and creatinine clearance. In high glucose incubated HK-2 cell, deacetylases activity of Sirt1 was attenuated that leads to decreased activity of nuclear factor kappa B (NF-?B). NF-?B was demonstrated to regulate miR-29 expression by directly binding to its promotor. The data of luciferase assay showed that miR-29 directly targets to Keap1 mRNA. While high glucose induced down regulation of miR-29 contributed to enhancement of Keap1 expression that finally reduced Nrf2 content by ubiquitinating Nrf2. Additionally, overexpression of miR-29 effectively relieved high glucose-reduced cell viability. CONCLUSION: High glucose induces renal tubular epithelial injury via Sirt1/NF-?B/microR-29/Keap1 signal pathway. |3' Untranslated Regions [MESH] |Animals [MESH] |Cell Survival [MESH] |Chromatin Immunoprecipitation [MESH] |Creatinine/blood [MESH] |Diabetes Mellitus, Experimental/metabolism/pathology [MESH] |Diabetic Nephropathies/metabolism [MESH] |Disease Models, Animal [MESH] |Epithelial Cells/*metabolism [MESH] |Glucose/*metabolism [MESH] |Intracellular Signaling Peptides and Proteins/*metabolism [MESH] |Kelch-Like ECH-Associated Protein 1 [MESH] |Kidney Tubules/cytology/*pathology [MESH] |Male [MESH] |MicroRNAs/*metabolism [MESH] |NF-E2-Related Factor 2/metabolism [MESH] |NF-kappa B/*metabolism [MESH] |Neoplasm Proteins/metabolism [MESH] |Nucleocytoplasmic Transport Proteins/metabolism [MESH] |Rats [MESH] |Rats, Wistar [MESH] |Signal Transduction [MESH] |Sirtuin 1/*metabolism [MESH]High glucose induces renal tubular epithelial injury via Sirt1/NF-ka(epmc).pdf DeepDyve Pubget Overpricing