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Homeostasis with Inner Ear Specific Autophagy Deficit Model Mice

Research Project

Project/Area Number 15K20223
Research Category

Grant-in-Aid for Young Scientists (B)

Allocation TypeMulti-year Fund
Research Field Otorhinolaryngology
Research InstitutionKeio University

Principal Investigator

Kojima Takashi  慶應義塾大学, 医学部(信濃町), 共同研究員 (60528660)

Research Collaborator KANZAKI Sho  
FUJIOKA Masato  
MITSUI Ayano  
Project Period (FY) 2015-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2016: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2015: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords内耳 / オートファジー / 蝸牛 / 恒常性維持機能 / 音響負荷 / 加齢性難聴 / 内耳有毛細胞
Outline of Final Research Achievements

The purpose of this research was to identify the location and physiologic function of autophagy in the cochlea.
We tried to visualize autophagy-activated area in the cochlea. GFP-LC3 reporter mouse revealed autophagy-activation at the cochlear neuroepithelium including outer hair cell. Then, outer hair cell specific autophagy deficit model mouse showed progressive high-frequency hearing loss. Also, immunostaining with 4-HNE indicated the protective action of autophagy against oxidative stress in outer hair cell.
At outer hair cell, autophagy may maintain homeostasis to the external environment. Suppressive function of autophagy against oxidative stress may inhibit cellular aging in the cochlea.

Report

(3 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report

URL: 

Published: 2015-04-16   Modified: 2018-03-22  

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