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Profiling of Matrix Vesicles obtained from cells in various differentiation states.

Research Project

Project/Area Number 15K09303
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Kidney internal medicine
Research InstitutionKansai University of Health Sciences

Principal Investigator

Itoh Shunji  関西医療大学, 保健医療学部, 准教授 (50275351)

Co-Investigator(Kenkyū-buntansha) 鍵弥 朋子  関西医療大学, 保健医療学部, 助教 (50717650)
畑村 育次  関西医療大学, 保健医療学部, 教授 (80336883)
Project Period (FY) 2015-04-01 – 2018-03-31
Project Status Completed (Fiscal Year 2017)
Budget Amount *help
¥4,810,000 (Direct Cost: ¥3,700,000、Indirect Cost: ¥1,110,000)
Fiscal Year 2017: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2016: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2015: ¥2,600,000 (Direct Cost: ¥2,000,000、Indirect Cost: ¥600,000)
Keywords基質小胞 / 異所性石灰化 / 組織石灰化 / カルシウム代謝 / 骨代謝 / 石灰化異常
Outline of Final Research Achievements

Calcification is an essential process for the formation of hard tissues. And ectopic calcification causes many diseases. However, the mechanism of calcification has been not cleared yet. It has been unknown whether the mechanisms of normal and ectopic calcification are identical. To identify molecules constituting the MV and elucidate the calcification mechanism, we studied using ATDC5 cells. The calcification of ATDC5 in the differentiated state is stimulated by the addition of inorganic phosphorus (Pi). Our results showed that the MVs were formed in the undifferentiated state. It was suggested that ATDC5 cells formed both MV without calcification ability and MV with calcification ability, depend on their differentiation state. Moreover, when ATDC5 cells differentiating to the articular cartilage-like cell, MV formation was observed but their calcification was not observed. We compared the MVs of these differentiated states and identified molecules necessary for the calcification.

Report

(4 results)
  • 2017 Annual Research Report   Final Research Report ( PDF )
  • 2016 Research-status Report
  • 2015 Research-status Report
  • Research Products

    (7 results)

All 2017 2016 2015

All Presentation (7 results) (of which Int'l Joint Research: 1 results,  Invited: 1 results)

  • [Presentation] 分化状態に依存した軟骨細胞の石灰化メカニズム2017

    • Author(s)
      伊藤俊治、鍵弥朋子、畑村育次
    • Organizer
      2017年度生命科学系学会合同年次大会(ConBio2017)
    • Related Report
      2017 Annual Research Report
  • [Presentation] 低亜鉛が神経・筋に及ぼす影響のマウスを用いた予備的検討2017

    • Author(s)
      伊藤俊治、深澤洋滋、荒川裕也、紀平為子
    • Organizer
      第28回日本微量元素学会学術集会
    • Related Report
      2017 Annual Research Report
  • [Presentation] MicroRNAs characteristic to the high incidence area of ALS in the Kii Peninsula2017

    • Author(s)
      Yuya Arakawa, Shunji Itoh, Junko Kohmoto, Masaya Hironishi, Hidefumi Ito, Tameko Kihira
    • Organizer
      XXIII World Congress of Neurology
    • Related Report
      2017 Annual Research Report
    • Int'l Joint Research
  • [Presentation] 新規精巣形成因子Pspの欠損は精巣ヒストンのアセチル化に影響しアポトーシスを引き起こす2016

    • Author(s)
      伊藤俊治、鍵弥朋子、荒川裕也、畑村育次
    • Organizer
      第39回日本分子生物学会年会
    • Place of Presentation
      横浜市
    • Year and Date
      2016-11-30
    • Related Report
      2016 Research-status Report
  • [Presentation] Psp遺伝子の破壊は老齢マウスで腎臓の空胞化を引き起こす2015

    • Author(s)
      伊藤俊治、鍵弥朋子、荒川裕也、宇野誠、早田荘、椎崎和弘、畑村育次
    • Organizer
      BMB2015
    • Place of Presentation
      神戸市
    • Year and Date
      2015-12-02
    • Related Report
      2015 Research-status Report
  • [Presentation] Psp KO マウスは精巣形成不全を示す2015

    • Author(s)
      鍵弥朋子、伊藤俊治、荒川裕也、櫻井威織、櫻井悠加、椎崎和弘、畑村育次
    • Organizer
      BMB2015
    • Place of Presentation
      神戸市
    • Year and Date
      2015-12-01
    • Related Report
      2015 Research-status Report
  • [Presentation] 骨折治癒の分子メカニズム2015

    • Author(s)
      伊藤俊治
    • Organizer
      第17回日本スポーツ整復療法学会
    • Place of Presentation
      宝塚市
    • Year and Date
      2015-10-24
    • Related Report
      2015 Research-status Report
    • Invited

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Published: 2015-04-16   Modified: 2019-03-29  

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