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10.14814/phy2.12730 http://scihub22266oqcxt.onion/10.14814/phy2.12730 C4814887!4814887 !27033449     free     free     free Warning: file_get_contents(https://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=27033449 &cmd=llinks): Failed to open stream: HTTP request failed! 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High glucose induces platelet-derived growth factor-C via carbohydrate response element-binding protein in glomerular mesangial cells |pdf=|usr=}}{{27033449 }} gab.com Text High glucose induces platelet-derived growth factor-C via carbohydrate response element-binding protein in glomerular mesangial cells JO: Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27033449 #FOAvip Persistent high concentration of glucose causes cellular stress and damage in diabetes via derangement of gene expressions. We previously reported high glucose activates hypoxia-inducible factor-1?and downstream gene expression in mesangial cells, leading to an extracellular matrix expansion in the glomeruli. A glucose-responsive transcription factor carbohydrate response element-binding protein (ChREBP) is a key mediator for such perturbation of gene regulation. To provide insight into glucose-mediated gene regulation in mesangial cells, we performed chromatin immunoprecipitation followed byDNAmicroarray analysis and identified platelet-derived growth factor-C (PDGF-C) as a novel target gene of ChREBP In streptozotocin-induced diabetic mice, glomerular cells showed a significant increase inPDGF-C expression; the ratio ofPDGF-C-positive cells to the total number glomerular cells demonstrated more than threefold increase when compared with control animals. In cultured human mesangial cells, high glucose enhanced expression ofPDGF-C protein by 1.9-fold. Knock-down of ChREBPabrogated this induction response. UpregulatedPDGF-C contributed to the production of typeIVand typeVIcollagen, possibly via an autocrine mechanism. Interestingly, urinaryPDGF-C levels in diabetic model mice were significantly elevated in a fashion similar to urinary albumin. Taken together, we hypothesize that a high glucose-mediated induction ofPDGF-C via ChREBPin mesangial cells contributes to the development of glomerular mesangial expansion in diabetes, which may provide a platform for novel predictive and therapeutic strategies for diabetic nephropathy. Twit Text FOAVip High glucose induces platelet-derived growth factor-C via carbohydrate response element-binding protein in glomerular mesangial cells ????Physiol Rep http://www.kidney.de/pget.php?&tw=1&pmid=27033449 #FOAvip Twit Text # Free Paper on # # # # # LINK http://www.kidney.de/pget.php?&tw=1&pmid=27033449 #FOAvip English Wikipedia <ref>{{Cite pmid|27033449 }}</ref> High glucose induces platelet-derived growth factor-C via carbohydrate response element-binding protein in glomerular mesangial cells #MMPMID27033449 Kitsunai H ; Makino Y ; Sakagami H ; Mizumoto K ; Yanagimachi T ; Atageldiyeva K ; Takeda Y ; Fujita Y ; Abiko A ; Takiyama Y ; Haneda M Physiol Rep 2016[Mar]; 4 (6 ): ä PMID27033449 show ga Persistent high concentration of glucose causes cellular stress and damage in diabetes via derangement of gene expressions. We previously reported high glucose activates hypoxia-inducible factor-1?and downstream gene expression in mesangial cells, leading to an extracellular matrix expansion in the glomeruli. A glucose-responsive transcription factor carbohydrate response element-binding protein (ChREBP) is a key mediator for such perturbation of gene regulation. To provide insight into glucose-mediated gene regulation in mesangial cells, we performed chromatin immunoprecipitation followed byDNAmicroarray analysis and identified platelet-derived growth factor-C (PDGF-C) as a novel target gene of ChREBP In streptozotocin-induced diabetic mice, glomerular cells showed a significant increase inPDGF-C expression; the ratio ofPDGF-C-positive cells to the total number glomerular cells demonstrated more than threefold increase when compared with control animals. In cultured human mesangial cells, high glucose enhanced expression ofPDGF-C protein by 1.9-fold. Knock-down of ChREBPabrogated this induction response. UpregulatedPDGF-C contributed to the production of typeIVand typeVIcollagen, possibly via an autocrine mechanism. Interestingly, urinaryPDGF-C levels in diabetic model mice were significantly elevated in a fashion similar to urinary albumin. Taken together, we hypothesize that a high glucose-mediated induction ofPDGF-C via ChREBPin mesangial cells contributes to the development of glomerular mesangial expansion in diabetes, which may provide a platform for novel predictive and therapeutic strategies for diabetic nephropathy. |Animals [MESH] |Basic Helix-Loop-Helix Leucine Zipper Transcription Factors/genetics/*metabolism [MESH] |Binding Sites [MESH] |Blood Glucose/*metabolism [MESH] |Cell Line [MESH] |Collagen Type IV/genetics/metabolism [MESH] |Collagen Type VI/genetics/metabolism [MESH] |Diabetes Mellitus, Experimental/blood/*complications [MESH] |Diabetic Nephropathies/blood/*etiology/pathology/urine [MESH] |Humans [MESH] |Lymphokines/genetics/*metabolism/urine [MESH] |Male [MESH] |Mesangial Cells/*metabolism/pathology [MESH] |Mice [MESH] |Mice, Inbred C57BL [MESH] |Nuclear Proteins/genetics/*metabolism [MESH] |Platelet-Derived Growth Factor/genetics/*metabolism/urine [MESH] |Promoter Regions, Genetic [MESH] |Protein Binding [MESH] |RNA Interference [MESH] |Time Factors [MESH] |Transcription Factors/genetics/*metabolism [MESH] |Transfection [MESH]High glucose induces platelet-derived growth factor-C via carbohydrate(epmc).pdf DeepDyve Pubget Overpricing