2011 Fiscal Year Final Research Report
Elucidation of the mechanisms underlying podocyte injury through endoplasmic reticulum stress and Development of novel therapeutic strategies for glomerular diseases
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 |
Section | 一般 |
Research Field |
Kidney internal medicine
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Research Institution | The University of Tokyo |
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
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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 |
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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[Presentation] Identification & Characterization of a Novel OncogenicHIF-1 Target Involved in Renal Cell Carcinoma2011
Author(s)
Shoji K, Mimura I, Ohse T, Murayama T, Inagi R, Wada T, Tanaka T, Kume H, GotoA, Fujita T, Aburatani H, Kodama T, Nangaku M
Organizer
The 44th Annual Meeting of the American Society of Nephrology.
Place of Presentation
Philadelphia, U. S. A
Year and Date
2011-11-12
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