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Analysis of disease mechanism of growth impairment in Down syndrome using human iPS cells

Research Project

Project/Area Number 25461643
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Embryonic/Neonatal medicine
Research InstitutionOsaka University

Principal Investigator

ARAHORI HITOMI  大阪大学, 医学(系)研究科(研究院), 助教 (40379186)

Project Period (FY) 2013-04-01 – 2016-03-31
Project Status Completed (Fiscal Year 2015)
Budget Amount *help
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
Fiscal Year 2013: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Keywords成長障害 / 軟骨細胞 / ダウン症候群 / iPS細胞 / ゲノム編集 / 染色体異常症候群
Outline of Final Research Achievements

Down syndrome (DS) is the most common chromosomal aneuploidy, which is caused by the trisomy of chromosome 21. Among their various medical symptom, DS patients show impairment in the growth. To analyze the mechanism of this growth impairment in DS, we generated DS-specific human induced pluripotent stem cells (iPSCs) from the cord blood using Sendaivirus vector, and differentiated them to chondrocyte. Although chondrocyte was successfully differentiated from human iPSC, its percentage was not sufficient yet. On the other hand, fibroblasts derived from not only DS patients but also 13, 18 trisomy patients showed low proliferation rate and premature senescence. The premature senescence was accompanied by accelerated RNA / protein synthesis, followed by increased oxidative stress. This trisomy-induced stress can be a major cause of growth impairment in DS.

Report

(4 results)
  • 2015 Annual Research Report   Final Research Report ( PDF )
  • 2014 Research-status Report
  • 2013 Research-status Report
  • Research Products

    (3 results)

All 2016 2014

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (2 results)

  • [Journal Article] Systematic cellular disease models reveal synergistic interactions of trisomy 21 and GATA1 mutations in hematopoietic abnormalities2016

    • Author(s)
      K. Banno, S. Omori, K. Hirata, N. Nawa, N. Nakagawa, K. Nishimura, M. Ohtaka, M. Nakanishi, T. Sakuma, T. Yamamoto, T. Toki, E. Ito, T. Yamamoto, C. Kokubu, J. Takeda, H. Taniguchi, H. Arahori, K. Wada, Y. Kitabatake and K. Ozono
    • Journal Title

      Cell Reports

      Volume: 15 Issue: 6 Pages: 1-15

    • DOI

      10.1016/j.celrep.2016.04.031

    • NAID

      120007135439

    • Related Report
      2015 Annual Research Report
    • Peer Reviewed / Open Access
  • [Presentation] ダウン症候群における病態発症メカニズムの解明2014

    • Author(s)
      北畠 康司、坂野 公彦、平田 克弥、大森 早也佳、荒堀 仁美、松浪 桂、谷口 英俊、和田 和子、大薗 恵一
    • Organizer
      第117回日本小児科学会学術集会
    • Place of Presentation
      名古屋
    • Year and Date
      2014-04-11
    • Related Report
      2014 Research-status Report
  • [Presentation] 疾患特異的ヒトiPS細胞をもちいたダウン症候群の病態解析2014

    • Author(s)
      北畠 康司、坂野 公彦、大森 早也佳、平田 克弥、那波 伸敏、和田 和子、荒堀 仁美、谷口 英俊、大薗 恵一
    • Organizer
      第37回日本小児遺伝学会学術集会
    • Place of Presentation
      名古屋
    • Year and Date
      2014-04-10
    • Related Report
      2014 Research-status Report

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

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