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2022 Fiscal Year Final Research Report

Mechanism of dentin-pulp complex formation by mechanosensor control

Research Project

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Project/Area Number 16K11578
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Conservative dentistry
Research InstitutionFukuoka Dental College

Principal Investigator

Hatakeyama Junko  福岡歯科大学, 口腔歯学部, 講師 (50374947)

Co-Investigator(Kenkyū-buntansha) 城戸 瑞穂  佐賀大学, 医学部, 教授 (60253457)
阿南 壽  福岡歯科大学, 口腔歯学部, 病院顧問 (80158732)
Project Period (FY) 2016-04-01 – 2023-03-31
Keywords象牙芽細胞様細胞 / 機械刺激センサー / TRPV4
Outline of Final Research Achievements

Focusing on TRPV channels activated by mechanostress, the degree of calcification of dentinoblasts upon TRPV4 stimulation was examined. Gene and protein expression of TRPV4 was observed in KN-3 cells, a dentinoblast-like cell line derived from rat dental pulp, and no difference in cell proliferation was observed by addition of TRPV4 inhibitor or promoter. Alizarin red staining showed significant enhancement of calcification and increase in alkaline phosphatase activity with the addition of the promoter. On the other hand, the addition of inhibitors did not promote calcification and suppressed alkaline phosphatase activity. The mechanosensor TRPV4 may be involved in hard tissue formation of dentinoblast-like cells.

Translated with www.DeepL.com/Translator (free version)

Free Research Field

歯内治療学

Academic Significance and Societal Importance of the Research Achievements

本研究でTRPV4によるラット歯髄由来象牙芽細胞様細胞株の石灰化が促進された。この成果は、メカノセンサーのアンタゴニストやアゴニストを標的とした象牙質誘導能を有する修復材の創出のための基盤構築を図る一端となる。TRPV4を覆髄材に応用することで、デンティンブリッジの形成や修復象牙質の形成促進を目的として、TRPV4の作動薬あるいは拮抗剤を将来の齲蝕治療の戦略へと加えることが示唆される。メカノセンサーのアンタゴニストやアゴニストを標的とした象牙質誘導能を有する修復材の創出のための基盤構築を図る。

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Published: 2024-01-30  

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