G-CSF prevents progression of diabetic nephropathy in rat.
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 possi...
| Main Authors: | , , , , , , , |
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| Format: | Article |
| Language: | English |
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Public Library of Science (PLoS)
2013-01-01
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| Series: | PLoS ONE |
| Online Access: | http://europepmc.org/articles/PMC3805566?pdf=render |
| _version_ | 1818561309932781568 |
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| author | Byung-Im So Yi-Sun Song Cheng-Hu Fang Jun-Young Park Yonggu Lee Jeong Hun Shin Hyuck Kim Kyung-Soo Kim |
| author_facet | Byung-Im So Yi-Sun Song Cheng-Hu Fang Jun-Young Park Yonggu Lee Jeong Hun Shin Hyuck Kim Kyung-Soo Kim |
| author_sort | Byung-Im So |
| collection | DOAJ |
| description | 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. |
| first_indexed | 2024-12-14T00:49:11Z |
| format | Article |
| id | doaj.art-cb4bec2683874e43b37639c7cb64a30e |
| institution | Directory Open Access Journal |
| issn | 1932-6203 |
| language | English |
| last_indexed | 2024-12-14T00:49:11Z |
| publishDate | 2013-01-01 |
| publisher | Public Library of Science (PLoS) |
| record_format | Article |
| series | PLoS ONE |
| spelling | doaj.art-cb4bec2683874e43b37639c7cb64a30e2022-12-21T23:23:57ZengPublic Library of Science (PLoS)PLoS ONE1932-62032013-01-01810e7704810.1371/journal.pone.0077048G-CSF prevents progression of diabetic nephropathy in rat.Byung-Im SoYi-Sun SongCheng-Hu FangJun-Young ParkYonggu LeeJeong Hun ShinHyuck KimKyung-Soo KimBACKGROUND: 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.http://europepmc.org/articles/PMC3805566?pdf=render |
| spellingShingle | Byung-Im So Yi-Sun Song Cheng-Hu Fang Jun-Young Park Yonggu Lee Jeong Hun Shin Hyuck Kim Kyung-Soo Kim G-CSF prevents progression of diabetic nephropathy in rat. PLoS ONE |
| title | G-CSF prevents progression of diabetic nephropathy in rat. |
| title_full | G-CSF prevents progression of diabetic nephropathy in rat. |
| title_fullStr | G-CSF prevents progression of diabetic nephropathy in rat. |
| title_full_unstemmed | G-CSF prevents progression of diabetic nephropathy in rat. |
| title_short | G-CSF prevents progression of diabetic nephropathy in rat. |
| title_sort | g csf prevents progression of diabetic nephropathy in rat |
| url | http://europepmc.org/articles/PMC3805566?pdf=render |
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