| Project/Area Number |
24659744
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Tohoku University |
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Principal Investigator |
TAKATA YUSUKE 東北大学, 医学(系)研究科(研究院), 非常勤講師 (60623999)
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| Project Period (FY) |
2012-04-01 – 2014-03-31
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2013: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2012: ¥910,000 (Direct Cost: ¥700,000、Indirect Cost: ¥210,000)
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| Keywords | 脂肪酸結合タンパク質 / Fabp / 蝸牛 / 難聴 / 脂肪酸 / Fabp7 / 加齢性難聴 / 老人性難聴 / 内耳 |
|---|
| Research Abstract |
The fatty acid-binding proteins (Fabps) bind to fatty acids and mediate their uptake and transport, thereby regulating metabolic pathways and gene expression. In the mouse cochlea, Fabp3 and Fabp7 have been identified. However, the role of these Fabps remains unknown. Wild-type, Fabp3 KO, and Fabp7 KO mice on the C57BL/6 background were used. Auditory thresholds were measured by the ABR. Cochlear morphology was assessed via HE staining, immunostaining, and TEM. Transcriptome analysis was also performed. Fabp3 (-/-) mice exhibited no auditory phenotypes. In contrast, the ABR thresholds of Fabp7 (-/-) mice were significantly reduced compared to Fabp7 (+/+) mice at 12 months. The numbers of SG neurons and fibrocytes were remarkably preserved in Fabp7 (-/-) mice at 12 and 15 months. Transcriptome analysis indicated that Fabp7 deficiency caused up-regulation of carbohydrate metabolism-related genes and conversely caused down-regulation of lipid metabolism-related genes.
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