G-CSF Prevents Progression of Diabetic Nephropathy in Rat

Title
G-CSF Prevents Progression of Diabetic Nephropathy in Rat
Author
송이선
Keywords
COLONY-STIMULATING FACTOR; BONE-MARROW-TRANSPLANTATION; ACUTE MYOCARDIAL-INFARCTION; FOOT PROCESS EFFACEMENT; STEM-CELL MOBILIZATION; VERSUS-HOST-DISEASE; OLETF RATS; EXTRACELLULAR-MATRIX; RENAL-DISEASE; TGF-BETA
Issue Date
2013-10
Publisher
PUBLIC LIBRARY SCIENCE, 1160 BATTERY STREET, STE 100, SAN FRANCISCO, CA 94111 USA
Citation
PLoS ONE,2013,8(10) p1-10
Abstract
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)-1 beta, transforming growth factor (TGF)-beta 1, 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-beta 1 and type IV collagen and IL-1 beta 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.
URI
http://journals.plos.org/plosone/article?id=10.1371/journal.pone.0077048http://hdl.handle.net/20.500.11754/42207
ISSN
1932-6203
DOI
10.1371/journal.pone.0077048
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RESEARCH INSTITUTE[S](부설연구소) > ETC
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