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Publication
Role of the USF1 transcription factor in diabetic kidney disease.
Authors
Sanchez AP, Zhao J, You Y, Declèves AE, Diamond-Stanic M, Sharma K
Submitted By
Kumar Sharma on 6/7/2011
Status
Published
Journal
American journal of physiology. Renal physiology
Year
2011
Date Published
8/1/2011
Volume : Pages
301 : F271 - F279
PubMed Reference
21543418
Abstract
The predominant transcription factors regulating key genes in diabetic kidney
disease have not been established. The transcription factor upstream stimulatory
factor 1 (USF1) is an important regulator of glucose-mediated transforming
growth factor (TGF)-ß1 expression in mesangial cells; however, its role in the
development of diabetic kidney disease has not been evaluated. In the present
study, wild-type (WT; USF1 +/+), heterozygous (USF1 +/-), and homozygous (USF1
-/-) knockout mice were intercrossed with Akita mice (Ins2/Akita) to induce type
1 diabetes. Mice were studied up to 36 wk of age. The degree of hyperglycemia
and kidney hypertrophy were similar in all groups of diabetic mice; however, the
USF1 -/- diabetic mice had significantly less albuminuria and mesangial matrix
expansion than the WT diabetic mice. TGF-ß1 and renin gene expression and
protein were substantially increased in the WT diabetic mice but not in USF1 -/-
diabetic mice. The underlying pathway by which USF1 is regulated by high glucose
was investigated in mesangial cell culture. High glucose inhibited AMP-activated
protein kinase (AMPK) activity and increased USF1 nuclear translocation.
Activation of AMPK with AICAR stimulated AMPK activity and reduced nuclear
accumulation of USF1. We thus conclude that USF1 is a critical transcription
factor regulating diabetic kidney disease and plays a critical role in
albuminuria, mesangial matrix accumulation, and TGF-ß1 and renin stimulation in
diabetic kidney disease. AMPK activity may play a key role in high
glucose-induced regulation of USF1.
Investigators with authorship
Name
Institution
Kumar Sharma
University of California San Diego
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Please acknowledge all posters, manuscripts or scientific materials that were generated in part or whole using funds from the Diabetic Complications Consortium(DiaComp) using the following text:
Financial support for this work provided by the NIDDK Diabetic Complications Consortium (RRID:SCR_001415, www.diacomp.org), grants DK076169 and DK115255
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