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Deciphering structural and functional basis of age-dependent hearing loss by using intracellular Ca2+ dynamics

Research Project

Project/Area Number 26430099
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Laboratory animal science
Research InstitutionInstitute of Physical and Chemical Research

Principal Investigator

Minowa Osamu  国立研究開発法人理化学研究所, バイオリソースセンター, 開発研究員 (00181967)

Co-Investigator(Renkei-kenkyūsha) IKEDA KATUHISA  順天堂大学, 医学部, 教授 (70159614)
KAMIYA KAZUSAKU  順天堂大学, 医学部, 准教授 (10374159)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Keywords加齢性難聴 / 老人性難聴 / モデルマウス / カルシウム / ENU-ミュータジェネシス / ミュータント / マウス変異体 / マウスモデル
Outline of Final Research Achievements

To investigate the significance of mouse mutant as a model for age-related progressive deafness, analyzed were phenotypes of mutants causing calcium dynamics abnormality. These analyses showed a relation between rate of deafness progression and a location of mutation site within the molecule. Most of the development of the age-related hearing loss is consequence of hair cell loss, but the certain contribution of the functional decay was presumed. A correlation was suggested between the extent of this functional decay and the period until cell depletion onset.
To achieve the optimization of in vitro expression system for measuring kinetic data on all applicable mutants, we examined the conditions of the system. It is thought to be essential to find an explicit marker of the change leading to cellular aging caused by calcium dynamics alteration, by accumulating those in vitro kinetic data and in vivo comprehensive analysis results of the phenotypes, for understanding the whole process.

Report

(4 results)
  • 2016 Annual Research Report   Final Research Report ( PDF )
  • 2015 Research-status Report
  • 2014 Research-status Report
  • Research Products

    (2 results)

All 2017 2014

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (1 results) (of which Int'l Joint Research: 1 results)

  • [Journal Article] Deficiency of transcription factor Brn4 disrupts cochlear gap junction plaques in a model of DFN3 non-syndromic deafness.2014

    • Author(s)
      Kidokoro Y, Karasawa K, Minowa O, Sugitani Y, Noda T, Ikeda K, Kamiya K.
    • Journal Title

      PLoS One

      Volume: Sep 26;9(9)

    • Related Report
      2014 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] Deafness Model Phenotypes with Impaired Cellular Calcium Sequestration Implies Pathways Contribut- ing Progressive Deafness2017

    • Author(s)
      美野輪 治
    • Organizer
      ARO 40th Annual MidWinter Meeting
    • Place of Presentation
      Baltimore Marriott Waterfront, Baltimore
    • Related Report
      2016 Annual Research Report
    • Int'l Joint Research

URL: 

Published: 2014-04-04   Modified: 2018-03-22  

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