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Basic research to investigate the involvement of advanced glycation endproducts in the progression and exacerbate of periodontal disease in diabetes mellitus

Research Project

Project/Area Number 21K09901
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Review Section Basic Section 57030:Conservative dentistry-related
Research InstitutionNihon University

Principal Investigator

TANABE Natsuko  日本大学, 歯学部, 准教授 (10409097)

Co-Investigator(Kenkyū-buntansha) 鈴木 直人  日本大学, 歯学部, 教授 (10226532)
Project Period (FY) 2021-04-01 – 2024-03-31
Project Status Completed (Fiscal Year 2023)
Budget Amount *help
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2023: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2022: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2021: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Keywords終末糖化産物 / 骨芽細胞 / 炎症性メディエーター / TAGE / 歯周病 / LPS / NF-κB / 炎症性生理活性物質
Outline of Research at the Start

終末糖化産物(AGEs)の中で糖代謝の中間体のグルセルアルデヒドに由来するTAGEは毒性が強く,AGEs受容体(RAGE)を介して生理活性を示し,さまざまな生活習慣病の発症・進展に関わっていることが近年報告されている。そこで申請者らは,TAGE生成と関連が深い糖尿病と歯周病との関係に着目し, TAGEが歯周病の増悪・難治化に影響を与えているのではないかと考え,歯周病原菌内毒素LPSよって惹起した歯周組織の炎症に及ぼす影響をin vitroで細胞生物・分子生物学的に検索することで分子メカニズムを解明することを目的としている。

Outline of Final Research Achievements

AGEs are generated by the Maillard reaction between amino acids of proteins and reducing sugars such as glucose. They are produced and accumulated not only in foods but also in living organisms. In this study, we focused on the relationship between diabetes and periodontal disease, which is closely related to the generation of AGEs. We hypothesized that AGEs accumulated in the blood due to diabetes may be one of the factors affecting the exacerbation and refractoriness of periodontal disease in diabetic patients. The results showed that AGEs further exacerbate the inflammation promoted by the endotoxin LPS of Gram-negative bacteria, which are periodontal pathogens.

Academic Significance and Societal Importance of the Research Achievements

本研究は,AGEsが骨芽細胞でLPSによって誘導された炎症を増悪することをIL-1alpha、プロスタグランジンE2ならびにS100A9などの炎症性メディエーター発現の促進と促進するための分子制御機構の1つを明らかにした。これらの本研究成果は,高血糖状態によって生成されたAGEsが,歯周病での歯槽骨吸収の原因の1つであるLPSによる炎症を増悪させること,さらにその機構が明らかとなることによって,将来的に歯周病の治療や予防へ役立てる一考になると考える。

Report

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

    (8 results)

All 2024 2023

All Journal Article (2 results) (of which Peer Reviewed: 2 results,  Open Access: 2 results) Presentation (6 results) (of which Int'l Joint Research: 3 results)

  • [Journal Article] Low-Intensity Pulsed Ultrasound Induced Osteoblast Differentiation Mediated by the PYK2-ERK2 Signaling in MC3T3-E1 Cells.2024

    • Author(s)
      Utsu Akihisa、Tanabe Natsuko、Manaka Soichiro、Tomita Keiko、Ichikawa Risa、Ono Misae、Masai Yuma、Suzuki Naoto、Motoyoshi Mitsuru
    • Journal Title

      Journal of Hard Tissue Biology

      Volume: 33 Issue: 1 Pages: 47-54

    • DOI

      10.2485/jhtb.33.47

    • ISSN
      1341-7649, 1880-828X
    • Related Report
      2023 Annual Research Report
    • Peer Reviewed / Open Access
  • [Journal Article] Co-Stimulation of AGEs and LPS Induces Inflammatory Mediators through PLCγ1/JNK/NF-κB Pathway in MC3T3-E1 Cells2023

    • Author(s)
      Tanabe Natsuko、Tomita Keiko、Manaka Soichiro、Ichikawa Risa、Takayama Tadahiro、Kawato Takayuki、Ono Misae、Masai Yuma、Utsu Akihisa、Suzuki Naoto、Sato Shuichi
    • Journal Title

      Cells

      Volume: 12 Issue: 10 Pages: 1383-1383

    • DOI

      10.3390/cells12101383

    • Related Report
      2023 Annual Research Report
    • Peer Reviewed / Open Access
  • [Presentation] AGEs reduced the expression of Claudin 4 and 7 in Ca9-22 cells.2024

    • Author(s)
      R. Ichikawa , N. Tanabe , K. Tomita , M. Ono , Y. Masai ,S. Manaka , A. Utsu , N. Suzuki , S. Sato
    • Organizer
      102nd General Session & Exhibition of the IADR(
    • Related Report
      2023 Annual Research Report
    • Int'l Joint Research
  • [Presentation] AGEs and LPS induces inflammatory mediators through PLCγ1/JNK/NF-κB pathway2024

    • Author(s)
      K. Tomita , N. Tanabe , R. Ichikawa , S. Manaka , A. Utsu ,N. Suzuki , S. Sato
    • Organizer
      102nd General Session & Exhibition of the IADR
    • Related Report
      2023 Annual Research Report
    • Int'l Joint Research
  • [Presentation] LIPUS Promotes Osteoblast Differentiation Mediated by PYK2-ERK Pathway in Osteoblasts2024

    • Author(s)
      A. Utsu, N. Tanabe, K. Tomita, R. Ichikawa, Y. Masai1, S. Manaka, M. Ono, N. Suzuki, M. Motoyoshi
    • Organizer
      102nd General Session & Exhibition of the IADR
    • Related Report
      2023 Annual Research Report
    • Int'l Joint Research
  • [Presentation] AGEs は p- PLCγ1 NF-κB の活性化を介して骨芽細胞の PGE2 および IL-1α 産生を促進する2023

    • Author(s)
      富田 景子, 田邉 奈津子, 髙山 忠裕, 間中 総一郎, 市川 理沙, 正井 佑篤, 汐見 登, 大塩 薫里, 鈴木 直人, 佐藤秀一
    • Organizer
      第66回春季日本歯周病学会学術大会
    • Related Report
      2022 Research-status Report
  • [Presentation] ヒト歯肉上皮細胞株Ca9-22細胞の上皮バリア機能に及ぼすAGEsの影響2023

    • Author(s)
      市川理沙、田邉奈津子、富田景子、高山忠弘、鈴木直人、佐藤秀一、齋藤 政一、八木 宏明
    • Organizer
      第66回春季日本歯周病学会学術大会
    • Related Report
      2022 Research-status Report
  • [Presentation] ヒト歯肉上皮細胞株Ca9-22細胞が上皮バリア機能に及ぼすAGEsの影響2023

    • Author(s)
      市川理沙,田邉奈津子,富田景子,小野美紗恵, 間中総一郎, 鈴木直人, 佐藤秀一
    • Organizer
      第75回 日本大学歯学会総会・学術大会
    • Related Report
      2022 Research-status Report

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

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