title: G-CSF prevents progression of diabetic nephropathy in rat.
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)-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.
authors.affiliation: Graduate School of Biomedical Science and Engineering, Hanyang University, Seoul, Korea.
authors.forename: Byung-Im
authors.initials: BI
authors.lastname: So
authors.forename: Yi-Sun
authors.initials: YS
authors.lastname: Song
authors.forename: Cheng-Hu
authors.initials: CH
authors.lastname: Fang
authors.forename: Jun-Young
authors.initials: JY
authors.lastname: Park
authors.forename: Yonggu
authors.initials: Y
authors.lastname: Lee
authors.forename: Jeong Hun
authors.initials: JH
authors.lastname: Shin
authors.forename: Hyuck
authors.initials: H
authors.lastname: Kim
authors.forename: Kyung-Soo
authors.initials: KS
authors.lastname: Kim
mesh_terms: D064591:Allografts; D000818:Animals; D001854:Bone Marrow Cells / Q000378:metabolism / Q000473:pathology; D016026:Bone Marrow Transplantation; D002465:Cell Movement / Q000187:drug effects; D024142:Collagen Type VI / Q000096:biosynthesis; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D003928:Diabetic Nephropathies / Q000378:metabolism / Q000473:pathology / Q000517:prevention & control*; D005786:Gene Expression Regulation / Q000187:drug effects; D050533:Glomerular Basement Membrane / Q000378:metabolism / Q000473:pathology; D005919:Glomerular Filtration Rate / Q000187:drug effects; D016179:Granulocyte Colony-Stimulating Factor / Q000494:pharmacology*; D053583:Interleukin-1beta / Q000096:biosynthesis; D050199:Podocytes / Q000378:metabolism / Q000473:pathology; D051381:Rats; D020334:Rats, Inbred OLETF; D053773:Transforming Growth Factor beta1 / Q000096:biosynthesis
chemical_list: D024142:Collagen Type VI; D053583:Interleukin-1beta; D053773:Transforming Growth Factor beta1; D016179:Granulocyte Colony-Stimulating Factor