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The role of Foxf1a for the function of hematopoietic stem cells

Research Project

Project/Area Number 26461452
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Hematology
Research InstitutionJichi Medical University

Principal Investigator

Ohmori Tsukasa  自治医科大学, 医学部, 教授 (70382843)

Co-Investigator(Kenkyū-buntansha) 窓岩 清治  自治医科大学, 医学部, 講師 (70296119)
西村 智  自治医科大学, 医学部, 教授 (80456136)
Project Period (FY) 2014-04-01 – 2017-03-31
Project Status Completed (Fiscal Year 2016)
Budget Amount *help
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2016: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2015: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2014: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Keywords造血幹細胞 / Niche / 細胞周期 / 転写因子 / 造血幹細胞ニッチ
Outline of Final Research Achievements

We previously reported that Vinculin is indispensable for the maintenance of hematopoietic stem cells (HSCs). Microarray analysis revealed that the expression of Foxf1a significantly reduced by the inhibition of vinculin. To examine the role of Foxf1a for HSC function, we developed conditional gene-deficient mice. In bone marrow, HSC and megakaryocytes expressed FoxF1a. While white blood cells, red blood cells, and platelets in peripheral blood were not affected, the number of bone marrow cells increased by the deletion of Foxf1a. Competitive repopulation assay of HSC showed that the deletion of Foxf1 deteriorated repopulation capacity of HSCs to reconstitute hematopoiesis. The frequency of long-term culture initiating cells also reduced. Finally, cell cycle analysis by the incorporation of BrdU in vivo revealed the increase in S phase of HSCs by the loss of Foxf1a. These data suggest that Foxf1a regulates quiescent of HSC in bone marrow niche to maintain the hematopoiesis.

Report

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

    (5 results)

All 2017 2016

All Presentation (4 results) (of which Int'l Joint Research: 1 results,  Invited: 3 results) Patent(Industrial Property Rights) (1 results)

  • [Presentation] CRISPR/Cas9-Mediated Genome Editing using an AAV8 Vector Improves Hemostasis in a Mouse Model of Hemophilia B in vivo2017

    • Author(s)
      Ohmori T
    • Organizer
      The 25thUS-Japan Cellular and Gene Therapy Conference
    • Place of Presentation
      U.S. Food and Drug Administration(Silver Spring, MD, USA)
    • Related Report
      2016 Annual Research Report
    • Int'l Joint Research / Invited
  • [Presentation] 血友病治療をサイエンスから考える2016

    • Author(s)
      大森 司
    • Organizer
      日本血栓止血学会教育セミナー
    • Place of Presentation
      クロスウエーブ梅田(大阪府・大阪市)
    • Year and Date
      2016-10-29
    • Related Report
      2016 Annual Research Report
    • Invited
  • [Presentation] 血友病遺伝子治療の現状と展望2016

    • Author(s)
      大森 司
    • Organizer
      第38回 日本血栓止血学会学術集会
    • Place of Presentation
      奈良春日野国際フォーラム(奈良県・奈良市)
    • Year and Date
      2016-06-16
    • Related Report
      2016 Annual Research Report
    • Invited
  • [Presentation] Forkhead box転写因子Foxf1aは血小板インテグリンの発現・機能に関与しない2016

    • Author(s)
      大森 司、西村 智、富永 眞一
    • Organizer
      平成28年度 日本生化学会関東支部例会
    • Place of Presentation
      自治医科大学教育研究棟(栃木県・下野市)
    • Related Report
      2016 Annual Research Report
  • [Patent(Industrial Property Rights)] 肝臓ゲノム上の凝固関連因子遺伝子を破壊するためのAAVベクター2017

    • Inventor(s)
      大森 司、他
    • Industrial Property Rights Holder
      学校法人自治医科大学
    • Industrial Property Rights Type
      特許
    • Filing Date
      2017-01-13
    • Related Report
      2016 Annual Research Report

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

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