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Decrease of FGF receptor (FGFR) and interstitial fibrosis in the kidney of streptozotocin-induced diabetic rats
M F Cheng1, L J Chen2, M C Wang1
1Division of Nephrology, Department of Internal Medicine, National Cheng Kung University Hospital, Tainan City, Taiwan.
Hormone and Metabolic Research = Hormon- Und Stoffwechselforschung = Hormones Et Metabolisme
|July 6, 2013
Summary
Reducing oxidative stress with tiron can reverse kidney fibrosis and restore fibroblast growth factor receptor (FGFR) expression in diabetic rats, independent of blood glucose levels.
Area of Science:
- Nephrology
- Endocrinology
- Cell Biology
Background:
- Fibrosis is a hallmark of end-stage renal disease.
- The fibroblast growth factor (FGF) 23-klotho axis may suppress renal fibrosis.
- Klotho expression is decreased in diabetic nephropathy, but the role of FGF in renal fibrosis remains unclear.
Purpose of the Study:
- To investigate the effect of hyperglycemia on FGF receptor (FGFR) and renal fibrosis in diabetic nephropathy.
- To explore the underlying mechanisms in cultured kidney cells.
Main Methods:
- Streptozotocin-induced diabetic rats (STZ rats) were treated with insulin or phloridzin.
- Madin-Darby Canine Kidney (MDCK) cells were exposed to high glucose, hydrogen peroxide, or tiron.
- Klotho was silenced using siRNA in MDCK cells.
Main Results:
- Insulin and phloridzin reversed fibrosis and FGFR expression in STZ rats and high glucose-exposed MDCK cells.
- Klotho silencing did not affect FGFR levels.
- Tiron restored FGFR expression and improved renal fibrosis in both MDCK cells and diabetic rats, irrespective of blood glucose control.
Conclusions:
- Interstitial fibrosis and decreased FGFR expression are characteristic of diabetic rat kidneys.
- Reducing oxidative stress via tiron can improve FGFR expression and renal fibrosis.
- Klotho does not influence FGFR expression in this context.
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