| Project/Area Number |
15390265
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Kidney internal medicine
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| Research Institution | Tokyo Medical and Dental University |
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Principal Investigator |
TERADA Yoshio Tokyo Medical and Dental University, Associate Professor, 医学部附属病院, 助教授 (30251531)
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| Co-Investigator(Kenkyū-buntansha) |
INOSHITA Seiji Tokyo Medical and Dental University, Assistant Professor, 医学部附属病院, 助手 (00345307)
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| Project Period (FY) |
2003 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥14,700,000 (Direct Cost: ¥14,700,000)
Fiscal Year 2006: ¥2,100,000 (Direct Cost: ¥2,100,000)
Fiscal Year 2005: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2004: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2003: ¥5,400,000 (Direct Cost: ¥5,400,000)
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| Keywords | Kidney / Regeneration / Renal tubule / Acute renal failure / Stem cell / Differentiation / Notch / Delta / 糸球体 / 慢性腎不全 / Ets-1 / Wnt-4 / HGF / Activin / cyclin D / cyclin A / 細胞周期 / ES細胞 / AQP2 / 足突起細胞 / Nephrin / Podocin |
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| Research Abstract |
Ischemic acute renal failure (ARF) is the most common form of ARF in the adult population. The molecular mechanisms of tubular regeneration after ischemic renal injury remain largely unknown. It has been suggested that regeneration processes may recapitulate developmental processes in order to restore organ or tissue function. The adult tubular epithelial cells have a potent ability of regenerate after cellular damage. We examined functional role of two developmental genes, Wnt-4 and Ets-1 in renal tubular regeneration in ARF. This slide shows hypothesis of mechanisms of renal tubular regeneration. After renal tubular injury, such as ischemia, renal tubular cells falls into apoptosis or necrosis. Then, some parts of injured renal tubules regenerate. We hypothesized three possibilities of renal tubular regeneration. One is the presence of renal tubular stem cells. Concerning to the stem cells, mamy presentation have already been reported in this meeting. The second possibility is Dedifferentiation. Our hypothesis is that the renal tubular cells transform to dedifferentiated cells, which have embryonic character, such as expression of Wnt-4 and Ets-1. The other possibility is involvement of blood cells.
In summary, we demonstrated that when the renal tubular cells are damaged, several recovery mechanisms are occurs using many types of stem cells. We may improve the recovery of renal tubular damage by manipulating stem cells such as tissue specific stem cells, or dedifferentiated stem cells, bone-marrow deribed stein cells, or ES cells. Further understanding of renal regeneration will improve new therapeutic strategy for ARF.
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