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G-CSF prevents progression of diabetic nephropathy in rat
Byung-Im So1, Yi-Sun Song, Cheng-Hu Fang
1Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
Background:
The protective effects of granulocyte colony-stimulating factor (G-CSF) have been demonstrated in a variety of renal disease models. However, the influence of G-CSF on diabetic nephropathy (DN) remains to be examined. In this study, we investigated the effect of G-CSF on DN and its possible mechanisms in a rat model.
Methods:
Otsuka Long-Evans Tokushima Fatty (OLETF) rats with early DN were administered G-CSF or saline intraperitoneally. Urine albumin creatinine ratio (UACR), creatinine clearance, mesangial matrix expansion, glomerular basement membrane (GBM) thickness, and podocyte foot process width (FPW) were measured. The levels of interleukin (IL)-1β, transforming growth factor (TGF)-β1, and type IV collagen genes expression in kidney tissue were also evaluated. To elucidate the mechanisms underlying G-CSF effects, we also assessed the expression of G-CSF receptor (G-CSFR) in glomeruli as well as mobilization of bone marrow (BM) cells to glomeruli using sex-mismatched BM transplantation.
Results:
After four weeks of treatment, UACR was lower in the G-CSF treatment group than in the saline group (p<0.05), as were mesangial matrix expansion, GBM thickness, and FPW (p<0.05). In addition, the expression of TGF-β1 and type IV collagen and IL-1β levels was lower in the G-CSF treatment group (p<0.05). G-CSFR was not present in glomerular cells, and G-CSF treatment increased the number of BM-derived cells in glomeruli (p<0.05).
Conclusions:
G-CSF can prevent the progression of DN in OLETF rats and its effects may be due to mobilization of BM cells rather than being a direct effect.
Insights
Granulocyte colony-stimulating factor (G-CSF) treatment reduced markers of kidney damage in diabetic nephropathy (DN) rats. These protective effects appear to stem from bone marrow cell mobilization, not direct action on kidney cells.
Area of Science:
- Nephrology
- Endocrinology
- Hematology
Background:
- Granulocyte colony-stimulating factor (G-CSF) shows protective effects in various kidney disease models.
- The impact of G-CSF on diabetic nephropathy (DN) has not been extensively studied.
- This research investigates G-CSF's effects and mechanisms in a rat model of DN.
Purpose of the Study:
- To determine the therapeutic effect of G-CSF on diabetic nephropathy (DN) in Otsuka Long-Evans Tokushima Fatty (OLETF) rats.
- To elucidate the underlying mechanisms of G-CSF action in DN.
- To assess G-CSF's influence on renal function and histological damage.
Main Methods:
- OLETF rats with early DN received G-CSF or saline treatment.
- Evaluated urine albumin creatinine ratio (UACR), creatinine clearance, and kidney histology (mesangial expansion, GBM thickness, podocyte foot process width).
- Assessed gene expression of IL-1β, TGF-β1, type IV collagen, and G-CSF receptor (G-CSFR) in kidney tissue; utilized bone marrow transplantation to track cell origins.
Main Results:
- G-CSF treatment significantly reduced UACR, mesangial matrix expansion, GBM thickness, and podocyte foot process width (p<0.05).
- Kidney tissue showed decreased expression of TGF-β1, type IV collagen, and IL-1β in the G-CSF group (p<0.05).
- G-CSF treatment increased the number of bone marrow-derived cells in glomeruli, with no detectable G-CSFR in glomerular cells.
Conclusions:
- G-CSF effectively prevents the progression of diabetic nephropathy in OLETF rats.
- The renoprotective effects of G-CSF are likely mediated by the mobilization of bone marrow cells.
- G-CSF does not appear to act directly on glomerular cells in this model.
