2013 Fiscal Year Final Research Report
Development of novel therapy against oxidative stress-induced inner ear damage
| Project/Area Number |
23592504
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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 |
Otorhinolaryngology
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| Research Institution | National Defense Medical College |
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Principal Investigator |
MATSUNOBU TAKESHI 防衛医科大学校(医学教育部医学科進学課程及び専門課程、動物実験施設、共同利用研究, 医学教育部医学科専門課程, 准教授 (00332205)
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| Co-Investigator(Kenkyū-buntansha) |
SHIOTANI Akihiro 防衛医科大学校, 病院, 教授 (80215946)
SATO Yasushi 防衛医科大学校, 病院, 講師 (10505267)
SATO Shunichi 防衛医科大学校, 防衛医学研究センター, 准教授 (90502906)
KAWAUCHI Satoko 防衛医科大学校, 防衛医学研究センター, 助教 (20506505)
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| Project Period (FY) |
2011 – 2013
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| Keywords | 内耳性難聴 / レーザー / アポトーシス / 内耳保護効果 |
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| Research Abstract |
We show that ERK2 play an important role in regulating inner hair cell survival and NIHL in mice. We created conditional Erk2 knockout mice to delete the Erk2 gene primarily in the hair cells using Cre/loxP system. Resultant hair cell-specific Erk2 conditional knockout (hErk2 CKO) were viable and fertile with normal appearance. After noise exposure control mice demonstrated a moderate recovery of ABR threshold shifts, however, no significant recovery was found for hErk2 CKO mice. There was significant difference between hErk2 CKO and control mice in ABR threshold shift. Furthermore a significant lower survival rate of IHCs was observed of hErk2 CKO mice as compared to control mice. We found that hErk2 CKO mice exhibited an increased sensitivity to noise exposure, suggesting that ERK2 plays an important role in protecting the inner hair cells from noise exposure.
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