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Analysis of non-code RNAs and transcription factors for the regulation of collagen gene expression in the microenvironment of the hard tissues.

Research Project

Project/Area Number 17K11848
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Surgical dentistry
Research InstitutionOita University

Principal Investigator

Yoshioka Hidekatsu  大分大学, 医学部, 客員研究員 (00222430)

Co-Investigator(Kenkyū-buntansha) 松尾 哲孝  大分大学, 医学部, 准教授 (10284788)
佐々木 隆子  大分大学, 医学部, 客員研究員 (30133193)
矢野 博之  大分大学, 医学部, 客員研究員 (50448552)
Project Period (FY) 2017-04-01 – 2023-03-31
Project Status Completed (Fiscal Year 2022)
Budget Amount *help
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2019: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2018: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Keywordsコラーゲン発現 / 非コードRNA / マイクロRNA / 長鎖非コードRNA / 硬組織 / 細胞外マトリックス / circ(環状)RNA / コラーゲン遺伝子 / 遺伝子発現 / 遺伝子発現調節 / コラーゲン / 転写因子 / 微小環境
Outline of Final Research Achievements

Collagens are major constituents of microenvironment of the hard tissues such as the bone and the dentin. Type I collagen with other minor type of collagens forms the collagen fibrils to perform cell proliferation and migration of the osteoblasts and the odontoblasts. The gene expression is regulated in the many steps. We have mainly investigated the transcriptional regulation of the collagen genes. In the present study, we examined translational gene regulation. Non-coding-protein RNAs, microRNA, long non-coding RNA, and circular RNA, regulate the gene expression. MicroRNAs are approximately 20-25 nucleotides in length and act as negative regulators of target genes. The results showed that miR-29b regulates the Col5a1 gene expression through binding to the 3’UTR in the osteoblasts. lncRNAs, which are several hundred nucleotides in length, are also regulate the gene expression. The expression of type I collagen was thought to be regulated by a couple of lncRNAs.

Academic Significance and Societal Importance of the Research Achievements

コラーゲンは体タンパクの約30%を占め、特に硬組織の主成分であり、コラーゲン遺伝子からコラーゲン線維形成までのメカニズムを解明することは極めて重要である。コラーゲンは骨や歯の強度に直接関与するものであり、高齢化社会を迎え、骨粗鬆症や歯牙の劣化や喪失等が医療において問題視されるなかで、本研究はこれらの再生医療につながる研究である。

Report

(7 results)
  • 2022 Annual Research Report   Final Research Report ( PDF )
  • 2021 Research-status Report
  • 2020 Research-status Report
  • 2019 Research-status Report
  • 2018 Research-status Report
  • 2017 Research-status Report
  • Research Products

    (5 results)

All 2021 2020 2019 2018 2017

All Journal Article (1 results) (of which Peer Reviewed: 1 results) Presentation (4 results)

  • [Journal Article] The pro-a1(V) collagen gene (Col5a1) is coordinately regulated by miR-29b with core promoter in cultured cells.2018

    • Author(s)
      Zhang JJ, Yano H, Sasaki T, Matsuo N, Yoshioka H
    • Journal Title

      Connect Tissue Res

      Volume: 59 Pages: 263-273

    • DOI

      10.1080/03008207.2017.1370465

    • Related Report
      2018 Research-status Report
    • Peer Reviewed
  • [Presentation] 骨芽細胞分化における長鎖非コード(lnc)RNAの機能解析2021

    • Author(s)
      矢野博之、濱中良志、矢野真美、松尾哲孝、吉岡秀克
    • Organizer
      日本分子生物学会
    • Related Report
      2021 Research-status Report
  • [Presentation] 骨芽細胞分化における長鎖非コード(lnc)RNAの発現2020

    • Author(s)
      矢野博之、濱中良志、矢野真美、松尾哲孝、吉岡秀克
    • Organizer
      日本分子生物学会
    • Related Report
      2020 Research-status Report
  • [Presentation] 骨芽細胞における長鎖非コード(lnc)RNAの発現2019

    • Author(s)
      矢野博之、濱中良志、松尾哲孝、甲斐浩一、吉岡秀克
    • Organizer
      日本分子生物学会
    • Related Report
      2019 Research-status Report
  • [Presentation] The pro-a1(V) collagen gene (Col5a1) is coordinately regulated by mir-29b with core promoter in cultured cells.2017

    • Author(s)
      Juan Juan Zhang, Hiroyuki Yano, Takako Sasaki, Noritaka Matsuo, Hidekatsu Yoshioka
    • Organizer
      第49回日本結合組織学会
    • Related Report
      2017 Research-status Report

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Published: 2017-04-28   Modified: 2024-01-30  

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