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High glucose activates HIF-1-mediated signal transduction in glomerular mesangial cells through a carbohydrate response element binding protein
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High glucose activates HIF-1-mediated signal transduction in glomerular mesangial cells through a carbohydrate response element binding protein
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High glucose activates HIF-1-mediated signal transduction in glomerular mesangial cells through a carbohydrate response element binding protein
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Journal Article
High glucose activates HIF-1-mediated signal transduction in glomerular mesangial cells through a carbohydrate response element binding protein
2010
Overview
High glucose evokes a variety of signals in mesangial cells that alter cellular functions responsible for the development of diabetic glomerulopathy. The hypoxia-inducible factor-1α (HIF-1α) regulates cellular homeostasis under hypoxic conditions, but it also has pleiotropic effects in response to cellular stresses at normoxia. Here we determined whether HIF-1α has a role in the regulation of mesangial cells in hyperglycemia. In the streptozotocin-induced diabetic mouse model, glomerular mesangial cells had a significant increase in HIF-1α expression in the nucleus. In cultured mesangial cells, high glucose enhanced the expression of HIF-1α and its target genes known to be involved in the development of diabetic glomerulopathy. A glucose-responsive carbohydrate response element binding protein (ChREBP) was found to have a critical role in the transcriptional upregulation of HIF-1α and downstream gene expression in mesangial cells exposed to high glucose. Knockdown of HIF-1α or ChREBP in mesangial cells abrogated the high glucose-mediated perturbation of gene expression. Our results show that ChREBP and HIF-1α mediate gene regulation in mesangial cells. Further studies will be needed to find out whether these findings are relevant to the development of the diabetic nephropathy.
Publisher
Elsevier Inc,Nature Publishing Group,Elsevier Limited
Subject
/ Biological and medical sciences
/ Diabetes. Impaired glucose tolerance
/ Endocrine pancreas. Apud cells (diseases)
/ Etiopathogenesis. Screening. Investigations. Target tissue resistance
/ Gene Expression Regulation - drug effects
/ Hypoxia-Inducible Factor 1 - genetics
/ Hypoxia-Inducible Factor 1 - metabolism
/ Male
/ Mesangial Cells - metabolism
/ Mice
/ Nephrology. Urinary tract diseases
/ Response Elements - drug effects
/ Signal Transduction - drug effects
