| Project/Area Number |
16H07188
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Otorhinolaryngology
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| Research Institution | Juntendo University |
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Principal Investigator |
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| Project Period (FY) |
2016-08-26 – 2018-03-31
|
| Project Status |
Completed (Fiscal Year 2017)
|
| Budget Amount *help |
¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
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| Keywords | カベオリン / 難聴 / 有毛細胞 / 遺伝性難聴 / 内耳 / 外有毛細胞 / コルチ器 |
|---|
| Outline of Final Research Achievements |
Mutations in GJB2, which encodes connexin 26 (Cx26), a cochlear gap junction protein, represent a major cause of pre-lingual, non-syndromic deafness. The degeneration of the organ of Corti observed in Cx26 mutant-associated deafness is thought to be a secondary pathology of hearing loss.The mechanism underlying secondary outer hair cell (OHC) degeneration remains unknown. We analyzed transmission electron micrographs of OHCs. Ultrastructure of the plasma membrane of OHCs shows a significantly large number of caveolae or caveolar vesicles were associated with OHCs lateral wall in Cx26 deficient mice as compared with those in the control mice. This may indicate that excessive endocytosis occurs in the presence of this Cx26 mutation, leading to OHC degeneration.
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