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Construction of epithelial cell barriers through epithelial cell-dendritic cell crosstalk and its application to periodontal disease.

Research Project

Project/Area Number 21K16935
Research Category

Grant-in-Aid for Early-Career Scientists

Allocation TypeMulti-year Fund
Review Section Basic Section 57010:Oral biological science-related
Research InstitutionIwate Medical University

Principal Investigator

Ikezaki Shojiro  岩手医科大学, 歯学部, 講師 (00849276)

Project Period (FY) 2021-04-01 – 2024-03-31
Project Status Completed (Fiscal Year 2023)
Budget Amount *help
¥3,380,000 (Direct Cost: ¥2,600,000、Indirect Cost: ¥780,000)
Fiscal Year 2023: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2022: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2021: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Keywords付着上皮 / セマフォリン / 上皮細胞 / 免疫細胞 / 歯周病 / Rhoシグナル
Outline of Research at the Start

歯周病は口腔常在菌を原因菌とする慢性感染症である。その病態の進行にはバリア機能を果たす上皮細胞とT細胞や抗原提示細胞などの免疫細胞が関わっていると考えられている。我々のグループでは歯周組織における上皮細胞にセマフォリン(Sema)4A, 4Dが発現していること、Sema4Dのシグナルが上皮細胞の接着と分化を制御していることを明らかにしてきた。本研究では、これまでの成果を発展させ、上皮細胞に加え樹状細胞におけるSema4Aの発現が細胞間接着に与える影響を調べることで歯周組織の恒常性とバリア機能の構築における、上皮-免疫担当細胞連携の役割を明らかにする。

Outline of Final Research Achievements

Periodontal disease is an inflammatory disease of periodontal tissues caused by periodontal pathogens, and junctional epithelium is involved in the defense mechanism. In this study, we focused on the mechanism of maintenance of the intercellular adhesion apparatus of junctional epithelium and investigated the effect of semaphorin (Sema). First, we established a mouse junctional epithelial cell line, mHAT-JE01, and confirmed that gene expression of occludin and Sema4A increased when co-cultured with mouse dendritic cells. Furthermore, we created junctional epithelial sheets and measured transepithelial electrical resistance (TEER), and found that the TEER value decreased in Rho kinase inhibition experiments. These results suggest that the junctional epithelium may autocrine-activate Sema4A to maintain the epithelial barrier.

Academic Significance and Societal Importance of the Research Achievements

付着上皮は歯肉において、外部環境からの異物侵入の障壁となる重要な構造である。この研究課題内で樹立した付着上皮細胞株は、細胞培養による歯周炎・付着上皮研究が発展するのに役立つと考えられる。また、実験結果から、免疫細胞である樹状細胞の新たな役割として付着上皮のバリア向上への関与が考えられた。現在の歯周病予防は、細菌要因・環境要因に重点を置いたものであるが、上皮細胞・免疫細胞にフォーカスした新たなアプローチの開発につながる研究である。

Report

(4 results)
  • 2023 Annual Research Report   Final Research Report ( PDF )
  • 2022 Research-status Report
  • 2021 Research-status Report
  • Research Products

    (4 results)

All 2023

All Journal Article (1 results) (of which Peer Reviewed: 1 results,  Open Access: 1 results) Presentation (3 results) (of which Int'l Joint Research: 1 results)

  • [Journal Article] A novel junctional epithelial cell line, mHAT-JE01, derived from incisor epithelial cells2023

    • Author(s)
      Ikezaki Shojiro、Otsu Keishi、Kumakami-Sakano Mika、Harada Hidemitsu
    • Journal Title

      Journal of Oral Biosciences

      Volume: 65 Issue: 1 Pages: 47-54

    • DOI

      10.1016/j.job.2023.01.004

    • Related Report
      2023 Annual Research Report 2022 Research-status Report
    • Peer Reviewed / Open Access
  • [Presentation] マウス付着上皮細胞培養系と細胞株の樹立2023

    • Author(s)
      池崎晶二郎、熊上(坂野)深香、大津圭史、原田英光
    • Organizer
      第128回 日本解剖学会総会・全国学術集会
    • Related Report
      2023 Annual Research Report 2022 Research-status Report
  • [Presentation] A novel junctional epithelial cell line, mHAT-JE01, derived from incisor epithelial cells2023

    • Author(s)
      Shojiro Ikezaki, Keishi Otsu, Mika Kumakami-Sakano, Hidemitsu Harada
    • Organizer
      International Seminar on Tooth Development and Regeneration
    • Related Report
      2023 Annual Research Report 2022 Research-status Report
    • Int'l Joint Research
  • [Presentation] Establishment of mouse junctional epithelial cells and culture system2023

    • Author(s)
      池崎晶二郎、高満正宜、新藤美湖、大津圭史、原田英光
    • Organizer
      第65回歯科基礎医学会学術大会
    • Related Report
      2023 Annual Research Report

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Published: 2021-04-28   Modified: 2025-01-30  

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