Investigation of TGF-signal transduction molecular mechanisms towards to inhibit the ankylosis

2021 Fiscal Year Final Research Report

• Project/Area Number: 19K19032
• Research Category: Grant-in-Aid for Early-Career Scientists
• Allocation Type: Multi-year Fund
• Review Section: Basic Section 57030:Conservative dentistry-related
• Research Institution: Kyushu University
• Principal Investigator: Mitarai Hiromi 九州大学, 大学病院, 助教 (60801660)
• Project Period (FY): 2019-04-01 – 2022-03-31
• Keywords: 歯根膜細胞 / α-SMA / TGF-β1

Outline of Final Research Achievements

We investigated α-SMA function, which is known to express in human PDL cells, and signaling pathway via TGF-β1. After ACTA2 knockdown using siRNA, in human PDL cell line 2-23, cell proliferation and migration were significantly downregulated. Also, after stimulating with TGF-β1, PDL-related gene expression, for example periostin and fibrillin1, was significantly downregulated compared with control cells. Collagen production was also significantly downregulated compared with control. Form western blotting analysis, we revealed that α-SMA knockdown significantly downregulated the phosphorylation of Smad2, Smad3 and YAP1. These results suggests that α-SMA involved in the function of PDL tissue and might be able to apply for periodontal regeneration therapy.

Free Research Field

歯根膜組織再生

Academic Significance and Societal Importance of the Research Achievements

意図的再植後にアンキローシスが生じると、正常な歯根膜感覚が消失し、置換性吸収を引き起こす可能性がある。しかしながら、アンキローシスの発生はコントロール困難であると考えられており、予知性の高い治療法への改善が必要とされている。本研究では、平滑筋細胞や創傷部など収縮性が高い組織に発現が報告されているα-SMAが歯根膜組織に発現し、その下流で制御するシグナルを解析する。α-SMA機能解析は咬合力緩衝機能を有する歯根膜組織再生に重要であり、今後の歯周組織再生療法への応用が期待される。