| Project/Area Number |
21591020
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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 |
Kidney internal medicine
|
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| Research Institution | The University of Tokyo |
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Principal Investigator |
WADA Takehiko 東京大学, 医学部附属病院, 助教 (90447409)
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| Co-Investigator(Kenkyū-buntansha) |
NANGAKU Masaomi 東京大学, 医学部附属病院, 特任講師 (90311620)
INAGI Reiko 東京大学, 医学部附属病院, 特任研究員 (50232509)
TANAKA Tetsuhiro 東京大学, 保健健康推進本部, 助教 (90508079)
|
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| Co-Investigator(Renkei-kenkyūsha) |
OHSE Takamoto 東京大学, 医学部附属病院, 助教 (10568447)
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| Project Period (FY) |
2009 – 2011
|
| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2011: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | 腎臓学 / 糸球体足細胞 / 小胞体ストレス / 蛋白尿 / アポトーシス / 分子シャペロン / 低酸素 / グルコース / 虚血再灌流モデル |
|---|
| Research Abstract |
We investigated the implication of endoplasmic reticulum(ER) stress in the process of podocyte injury. Cultured growth-restrictive podocytes showed enhanced unfolded protein response under hypoxia, one of the metabolic stresses we tested. The apoptosis pathway associated with CHOP, which is one of the ER stress-related molecules, included a complicated network with Bcl-2-related proteins. Furthermore, we found that methylglyoxal, a carbonyl compound, directly damaged podocytes. Those results suggest that hypoxia, ER stress and carbonyl stress may have a crosstalk with each other and promote podocyte injury.
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