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Cell therapy using iPS derived cells for hearing loss against the degenerations of various cochlear cell types

Research Project

Project/Area Number 25670721
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Otorhinolaryngology
Research InstitutionJuntendo University

Principal Investigator

IKEDA Katsuhisa  順天堂大学, 医学部, 教授 (70159614)

Co-Investigator(Kenkyū-buntansha) KAMIYA Kazusaku  順天堂大学, 医学部, 准教授 (10374159)
IIZUKA Takashi  順天堂大学, 医学部, 助教 (40372932)
Project Period (FY) 2013-04-01 – 2015-03-31
Project Status Completed (Fiscal Year 2014)
Budget Amount *help
¥3,640,000 (Direct Cost: ¥2,800,000、Indirect Cost: ¥840,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Keywords聴覚障害 / 人工多能性幹細胞 / 内耳 / 有毛細胞 / ラセン神経節細胞 / 分化誘導 / 細胞治療 / 再生医療 / 遺伝性難聴 / iPS細胞 / 内耳前駆細胞 / 多能性幹細胞 / 幹細胞ホーミング / 内耳有毛細胞 / 蝸牛線維細胞
Outline of Final Research Achievements

In this study, we co-cultured iPS-derived cells with three different regions of the cochlear tissue and induced their differentiation into various types of inner cells. The number of Nanog-positive colonies with reporter GFP controlled by Nanog promotor was counted to assess the undifferentiated level of the cells. In the co-cultured cells with spiral ganglion, many cells with neurite-like protrusions were observed among the colonies. In the co-culture with the organ of Corti and spiral limbus (OC/SL), neuron-like cells were observed on the cell layer with tight junction-like adhesions. In the co-culture with the cochlear lateral wall, many cell layers with tight junction-like adhesions were observed, while undifferentiated Nanog-positive colonies were not observed. It was suggested that differentiation of iPS cells to cochlear cells was regulated depending on the part of the co-cultured organs.

Report

(3 results)
  • 2014 Annual Research Report   Final Research Report ( PDF )
  • 2013 Research-status Report
  • Research Products

    (6 results)

All 2015 2014 2013

All Journal Article (6 results) (of which Peer Reviewed: 6 results,  Open Access: 4 results,  Acknowledgement Compliant: 1 results)

  • [Journal Article] Perinatal Gjb2 gene transfer rescues hearing in a mouse model of hereditary deafness.2015

    • Author(s)
      Iizuka T, Kamiya K, Gotoh S, Sugitani Y, Suzuki M, Noda T, Minowa O, Ikeda K.
    • Journal Title

      Hum Mol Genet.

      Volume: epub

    • Related Report
      2014 Annual Research Report
    • Peer Reviewed / Open Access / Acknowledgement Compliant
  • [Journal Article] Assembly of the cochlear gap junction macromolecular complex requires connexin 26.2014

    • Author(s)
      Kamiya K, Yum SW, Kurebayashi N, Muraki M, Ogawa K, Karasawa K, Miwa A, Guo X, Gotoh S, Sugitani Y, Yamanaka H, Ito-Kawashima S, Iizuka T, Sakurai T, Noda T, Minowa O, Ikeda K.
    • Journal Title

      J Clin Invest,

      Volume: 124 Issue: 4 Pages: 1598-1607

    • DOI

      10.1172/jci67621

    • Related Report
      2014 Annual Research Report 2013 Research-status Report
    • Peer Reviewed / Open Access
  • [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: 9(9) Issue: 9 Pages: e108216-e108216

    • DOI

      10.1371/journal.pone.0108216

    • Related Report
      2014 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Dominant negative connexin26 mutation R75W causing severe hearing loss influences normal programmed cell death in postnatal organ of Corti2014

    • Author(s)
      Ayako Inoshita, Keiko Karasawa, Megumi Funakubo, Asuka Miwa, Katsuhisa Ikeda, Kazusaku Kamiya
    • Journal Title

      BMC genetics

      Volume: 15(1) Issue: 1 Pages: 1-8

    • DOI

      10.1186/1471-2156-15-1

    • Related Report
      2013 Research-status Report
    • Peer Reviewed / Open Access
  • [Journal Article] Treatment with 17-allylamino-17-demethoxygeldanamycin ameliorated symptoms of Bartter syndrome type caused by mutated Bsnd in mice.2013

    • Author(s)
      Nomura N, Kamiya K, Ikeda K, Yui N, Chiga M, Sohara E, Rai T, Sasaki S, Uchida S.
    • Journal Title

      Biochem Biophys Res Commun.

      Volume: 441 Issue: 3 Pages: 544-49

    • DOI

      10.1016/j.bbrc.2013.10.129

    • Related Report
      2013 Research-status Report
    • Peer Reviewed
  • [Journal Article] 遺伝性難聴への内耳細胞治療法開発 Cell therapy for hereditary hearing loss with stem cell homing factors.2013

    • Author(s)
      神谷和作
    • Journal Title

      日本薬理学雑誌

      Volume: 141(4) Pages: 191-4

    • Related Report
      2013 Research-status Report
    • Peer Reviewed

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Published: 2014-07-25   Modified: 2019-07-29  

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