| Project/Area Number |
22590880
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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 |
INAGI Reiko 東京大学, 医学部附属病院, 特任研究員 (50232509)
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|---|
| Co-Investigator(Kenkyū-buntansha) |
NANGAKU Masaomi 東京大学, 医学部附属病院, 教授 (90311620)
WADA Takehiko 東京大学, 医学部附属病院, 助教 (90447409)
OHSE Takamoto 東京大学, 医学部附属病院, 助教 (10568447)
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| Project Period (FY) |
2010 – 2012
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| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2012: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2011: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2010: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 小胞体ストレス / 尿細管 / unfolded protein response / 虚血 / 酸化ストレス / 翻訳制御 / microRNA / 腎臓病 / UPR経路 / 酸化ストリス / 腎臟病 |
|---|
| Research Abstract |
To assess the pathophysiological function of microRNA (miRNA) inchronic kidney disease (CKD), we performed the miRNA microarray analysis and the loss/gainfunction assay in human tubular cells (HK-2) expose to hypoxia-induced oxidative stressor endoplasmic reticulum (ER) stress. The results demonstrated that 1) miR-205 expressionwas significantly decreased by hypoxia-induced oxidative stress or ER stress and wasassociated with cellular sensitivity to the stresses, 2) PHD1, which degradestranscription factors (HIF, ATF4) of hypoxia and ER stress signals, is a target for miR-205,3) decreased miR-205 suppressed the expression of HIF/ATF4 downstream genes, anti-oxidantenzymes, via upregulation of PHD1. miR-205 might contribute to tubular homeostasis.
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