| Project/Area Number |
24500502
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Laboratory animal science
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| Research Institution | Tokyo Metropolitan Institute of Medical Science |
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Principal Investigator |
MATSUOKA Kunie 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, 主席研究員 (40291158)
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| Co-Investigator(Kenkyū-buntansha) |
KIKKAWA Yoshiaki 公益財団法人東京都医学総合研究所, ゲノム医科学研究分野, プロジェクトリーダー (20280787)
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| Project Period (FY) |
2012-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | 難聴 / 内耳外有毛細胞 / 疾患モデル / トランスジェニックマウス / ジフテリア毒素 / 外有毛細胞 |
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| Outline of Final Research Achievements |
Outer hair cells (OHC) play an essential role in the amplification of sound-induced vibrations in the cochlea. To study the critical functions of OHC, we generated a novel mouse model, OHC-TRECK, for hearing impairment by introducing the human diphtheria toxin (DT) receptor gene under the control of the mouse prestin promoter. DT administration to OHC-TRECK mice were found to result in severe hearing impairment with the decrease in amplitude of distortion product otoacoustic emissions and the elevated auditory brainstem responses thresholds. Microarray and RNA-seq analysis using inner ear cochlear RNA revealed that the expression of Oncomodulin (Ocm) gene, coding EF-hand Ca2+ binding protein, was significantly decreased in DT-administered OHC-TRECK mice and OCM expression was specifically detected in OHC. These results suggest that OCM performs an important function with Ca2+ binding ability in mechanotransduction in OHC.
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