| Project/Area Number |
22591880
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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 |
Otorhinolaryngology
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| Research Institution | Okayama University |
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Principal Investigator |
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| Co-Investigator(Kenkyū-buntansha) |
FUKUSHIMA Kunihiro 岡山大学, 岡山大学病院, 講師 (50284112)
KATAOKA Yuko 岡山大学, 岡山大学病院, 助教 (10362972)
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| Project Period (FY) |
2010 – 2012
|
| Project Status |
Completed (Fiscal Year 2012)
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| Budget Amount *help |
¥4,290,000 (Direct Cost: ¥3,300,000、Indirect Cost: ¥990,000)
Fiscal Year 2012: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2011: ¥650,000 (Direct Cost: ¥500,000、Indirect Cost: ¥150,000)
Fiscal Year 2010: ¥2,860,000 (Direct Cost: ¥2,200,000、Indirect Cost: ¥660,000)
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| Keywords | 急性感音難聴 / MAP kinase / 騒音性難聴モデルマウス / 騒音性難聴マウス / 音響外傷 / c-Jun / siRNA / c-jun / 騒音性難聴 / リアルタイムRT-PCR / アポトーシス / 内耳遺伝子治療 |
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| Research Abstract |
The involvement of MAP kinase in noise-induced hearing loss (NIHL) has been implicated in the cochlea; however, it was unknown how expression levels of MAP kinase change after the onset of NIHL and whether they are regulated by transient phosphorylation or protein synthesis.In the data of the present study, the phospho-MEK1/ ERK/p90RSK signaling pathway was activated in the spiral ligament and the sensory and supporting cells of the organ of Corti, with peaks at 3-6 h and independently of regulations of total-MEK1/ERK/p90RSK. The expression of phospho-JNK and p38MAPK showed late upregulation in spiral neurons at 48 h, in addition to early upregulations with peaks at 3 h after noise trauma. Phospho-p38MAPK activation was dependent on upregulation of total-p38MAPK. The present data provide a significant basis for future therapeutic strategies for acute sensorineural hearing loss, including those utilizing siRNA.
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