ArticleNephron. Experimental nephrology2011
High glucose upregulates upstream stimulatory factor 2 in human renal proximal tubular cells through angiotensin II-dependent activation of CREB.
Article in Nephron. Experimental nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 30 citations in OpenAlex.
- Angiotensin receptor blocker ameliorates the development of tubulointerstitial injury and fibrosis associated with tubular proteinuria observed in subclinical diabetic kidney disease.Frontiers in pharmacology · 2026Article
- Transcriptomic screening of novel targets of sericin in human hepatocellular carcinoma cells.Scientific reports · 2024Article
- β-LAPachone is renoprotective in streptozotocin-induced diabetic mice via regulating the PI3K/Akt/mTOR signaling pathway.Iranian journal of basic medical sciences · 2021Article
- Protective mechanism of apigenin in diabetic nephropathy is related to its regulation of miR-423-5P-USF2 axis.American journal of translational research · 2021Article
- Study of the Active Components and Molecular Mechanism ofFrontiers in molecular biosciences · 2021Article
- Glucose Induces IL-1α-Dependent Inflammation and Extracellular Matrix Proteins Expression and Deposition in Renal Tubular Epithelial Cells in Diabetic Kidney Disease.Frontiers in immunology · 2020Article
- Blockade of myeloid differentiation 2 attenuates diabetic nephropathy by reducing activation of the renin-angiotensin system in mouse kidneys.British journal of pharmacology · 2019Article
- High glucose augments angiotensinogen in human renal proximal tubular cells through hepatocyte nuclear factor-5.PloS one · 2017Article
- O-GlcNAcylation: a bridge between glucose and cell differentiation.Journal of cellular and molecular medicine · 2016Review
- Intrarenal renin-angiotensin system mediates fatty acid-induced ER stress in the kidney.American journal of physiology. Renal physiology · 2016Article
- Effect of Sodium-Glucose Co-Transporter 2 Inhibitor, Dapagliflozin, on Renal Renin-Angiotensin System in an Animal Model of Type 2 Diabetes.PloS one · 2016 · on this mapArticle
- Article
- Role of upstream stimulatory factor 2 in diabetic nephropathy.Frontiers in biology · 2015Article
- An angiotensin-(1-7) peptidase in the kidney cortex, proximal tubules, and human HK-2 epithelial cells that is distinct from insulin-degrading enzyme.American journal of physiology. Renal physiology · 2015Article
- Significant association between glycemic status and increased estimated postglomerular resistance in nondiabetic subjects - study of inulin and para-aminohippuric acid clearance in humans.Physiological reports · 2015Article
- Inhibition of MAPK-mediated ACE expression by compound C66 prevents STZ-induced diabetic nephropathy.Journal of cellular and molecular medicine · 2014Article
- TGF-β signaling in tissue fibrosis: redox controls, target genes and therapeutic opportunities.Cellular signalling · 2013Review
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
BACKGROUND/
aimsWe have previously demonstrated that a transcription factor, upstream stimulatory factor 2 (USF2), regulates glucose-induced thrombospondin 1 expression and transforming growth factor-β activity in mesangial cells, and plays an important role in diabetic glomerulopathy. In this study, we determined whether USF2 expression in renal proximal tubular cells is regulated by glucose and contributes to diabetic tubulointerstitial fibrosis.
methodsHuman renal proximal tubular cells (HK-2 cells) were treated with normal- or high-glucose medium for 24 h. After treatment, real-time PCR or immunoblotting was used to determine the expression of USF2 and other components of the renin-angiotensin system in HK-2 cells.
resultsHigh glucose upregulated USF2 expression and increased extracellular matrix accumulation in HK-2 cells; both were inhibited by siRNA-mediated USF2 knockdown. In addition, high glucose stimulated angiotensinogen and renin expression, increased renin activity, and resulted in increased angiotensin II formation. Treatment of HK-2 cells with an angiotensin II receptor 1 (AT1) blocker--losartan--prevented high-glucose-induced USF2 expression and high-glucose-enhanced phosphorylation of CREB (cAMP response element-binding protein).
conclusionOur data established that high glucose stimulated USF2 expression in HK-2 cells, at least in part, through angiotensin II-AT1-dependent activation of CREB, which can contribute to diabetic tubulointerstitial fibrosis.
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