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10.1038/srep45807 http://scihub22266oqcxt.onion/10.1038/srep45807 28374767!5379554!28374767     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=28374767&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 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 217.6 to int loses precision in C:\Inetpub\vhosts\kidney.de\httpdocs\pget.php on line 534       Sci+Rep 2017 ; 7 (ä): 45807 Nephropedia Template TP {{tp|p=28374767|t=2017. Transcription factors regulate GPR91-mediated expression of VEGF in hypoxia-induced retinopathy |pdf=|usr=}}{{28374767}} gab.com Text Transcription factors regulate GPR91-mediated expression of VEGF in hypoxia-induced retinopathy JO: Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28374767 #FOAvip Hypoxia is the most important factor in the pathogenesis of diabetic retinopathy (DR). Our previous studies demonstrated that G protein-coupled receptor 91(GPR91) participated in the regulation of vascular endothelial growth factor (VEGF) secretion in DR. The present study induced OIR model in newborn rats using exposure to alternating 24-hour episodes of 50% and 12% oxygen for 14 days. Treatment with GPR91 shRNA attenuated the retinal avascular area, abnormal neovascularization and pericyte loss. Western blot and qRT-PCR demonstrated that CoCl(2) exposure promoted VEGF expression and secretion, activated the ERK1/2 signaling pathways and upregulated C/EBP and AP-1. Knockdown of GPR91 inhibited ERK1/2 activity. GPR91 siRNA transduction and the ERK1/2 inhibitor U0126 inhibited the increases in C/EBP beta, C/EBP delta, c-Fos and HIF-1alpha. Luciferase reporter assays and a chromatin immunoprecipitation (ChIP) assay demonstrated that C/EBP beta and c-Fos bound the functional transcriptional factor binding site in the region of the VEGF promoter, but not C/EBP delta. Knockdown of C/EBP beta and c-Fos using RNAi reduced VEGF expression. Our data suggest that activation of the GPR91-ERK1/2-C/EBP beta (c-Fos, HIF-1alpha) signaling pathway plays a tonic role in regulating VEGF transcription in rat retinal ganglion cells. Twit Text FOAVip Transcription factors regulate GPR91-mediated expression of VEGF in hypoxia-induced retinopathy ????Sci Rep http://www.kidney.de/pget.php?&tw=1&pmid=28374767 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=28374767 #FOAvip English Wikipedia <ref>{{Cite pmid|28374767}}</ref> Transcription factors regulate GPR91-mediated expression of VEGF in hypoxia-induced retinopathy #MMPMID28374767 Li T; Hu J; Gao F; Du X; Chen Y; Wu Q Sci Rep 2017[Apr]; 7 (ä): 45807 PMID28374767show ga Hypoxia is the most important factor in the pathogenesis of diabetic retinopathy (DR). Our previous studies demonstrated that G protein-coupled receptor 91(GPR91) participated in the regulation of vascular endothelial growth factor (VEGF) secretion in DR. The present study induced OIR model in newborn rats using exposure to alternating 24-hour episodes of 50% and 12% oxygen for 14 days. Treatment with GPR91 shRNA attenuated the retinal avascular area, abnormal neovascularization and pericyte loss. Western blot and qRT-PCR demonstrated that CoCl(2) exposure promoted VEGF expression and secretion, activated the ERK1/2 signaling pathways and upregulated C/EBP and AP-1. Knockdown of GPR91 inhibited ERK1/2 activity. GPR91 siRNA transduction and the ERK1/2 inhibitor U0126 inhibited the increases in C/EBP beta, C/EBP delta, c-Fos and HIF-1alpha. Luciferase reporter assays and a chromatin immunoprecipitation (ChIP) assay demonstrated that C/EBP beta and c-Fos bound the functional transcriptional factor binding site in the region of the VEGF promoter, but not C/EBP delta. Knockdown of C/EBP beta and c-Fos using RNAi reduced VEGF expression. Our data suggest that activation of the GPR91-ERK1/2-C/EBP beta (c-Fos, HIF-1alpha) signaling pathway plays a tonic role in regulating VEGF transcription in rat retinal ganglion cells. |Animals[MESH] |Animals, Newborn[MESH] |Butadienes/administration & dosage[MESH] |CCAAT-Enhancer-Binding Protein-beta/*genetics[MESH] |CCAAT-Enhancer-Binding Protein-delta/genetics[MESH] |Cobalt/administration & dosage[MESH] |Diabetic Retinopathy/drug therapy/*genetics/pathology[MESH] |Gene Expression Regulation/drug effects[MESH] |Humans[MESH] |Hypoxia-Inducible Factor 1, alpha Subunit/genetics[MESH] |Hypoxia/*genetics/pathology[MESH] |MAP Kinase Signaling System/drug effects[MESH] |Neovascularization, Pathologic/genetics/pathology[MESH] |Nitriles/administration & dosage[MESH] |Proto-Oncogene Proteins c-fos/genetics[MESH] |Rats[MESH] |Receptors, G-Protein-Coupled/*genetics[MESH] |Retina/metabolism/pathology[MESH]Transcription factors regulate GPR91-mediated expression of VEGF in h(epmc).pdf DeepDyve Pubget Overpricing