| Project/Area Number |
21591420
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Embryonic/Neonatal medicine
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| Research Institution | Keio University |
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Principal Investigator |
HIDA Mariko 慶應義塾大学, 医学部, 共同研究員 (20276306)
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| Co-Investigator(Kenkyū-buntansha) |
AWAZU Midori 慶應義塾大学, 医学部, 講師 (20129315)
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| Project Period (FY) |
2009 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,250,000 (Direct Cost: ¥2,500,000、Indirect Cost: ¥750,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
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| Keywords | 胎児医学 / autophagy / エピジェネテイクス / oligonephronia / 子宮内発育遅滞 / ステロイド / 低栄養 / 成人病胎児期発症説(Barker仮説) / 腎発生 |
|---|
| Research Abstract |
The main purpose of this study is to elucidate the role of mTOR(The mammalian target of rapamycin) in developmental disorder of kidney induced by fetal programming. Maternal nutrient restriction(NR) or dexamethasone treatment(DEX) led to significant growth restriction and reduction of nephron number in fetal metanephros. Micro array of these metanephros revealed the NR and DEX had led to change in expression pattern of a large number of genes and proteins including mTOR pathways. Immunoblot and immunohistochemistry of metanephros, mTOR pathway was downregulated by NR and DEX. We are now analyzing the methylation pattern of some of the genes which expression alteration was detected in the micro array analysis. In conclusion, we have identified downregulation of mTOR pathway by NR or DEX, but the precise mechanism to be elucidated which may be important in the pathogenesis of fetal programming in kidney development.
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