Analysis of the mechanism of HIF1a-modulated production of inflammatory mediators in human dental pulp cells

2020 Fiscal Year Final Research Report

• Project/Area Number: 19K24137
• Research Category: Grant-in-Aid for Research Activity Start-up
• Allocation Type: Multi-year Fund
• Review Section: 0907:Oral science and related fields
• Research Institution: Tokyo Medical and Dental University
• Principal Investigator: Fujii Mayuko 東京医科歯科大学, 歯学部附属病院, 医員 (80844357)
• Project Period (FY): 2019-08-30 – 2021-03-31
• Keywords: 歯髄炎 / 低酸素 / HIF1a / LPS

Outline of Final Research Achievements

It is unclear how hypoxia modulates pulpitis. In this study, we stimulated human dental pulp cells with LPS and investigated inflammatory mediators and signaling pathways. We found that forced expression of HIF1a further enhanced LPS-stimulated activation of NFkB signaling and ｍRNA of inflammatory mediators such as IL1b and TNFa. On the other hand, IL6 production was induced by LPS stimulation, but suppressed by forced expression of HIF1a. In this study, we confirmed that SOCS3 is upregulated in the presence of HIF1a and is involved in the regulation of CEBP/b production under LPS stimulation.

Free Research Field

細菌性炎症

Academic Significance and Societal Importance of the Research Achievements

歯髄組織は健全な状態においても低酸素状態にあり、硬組織で囲まれているため、歯髄炎によりさらに低酸素状態が誘発される。HIF1aによって歯髄細胞からの炎症性メディエーター産生や炎症の病態がどのように修飾されているのか、HIF1aが関与する歯髄炎の特性を明らかにし、制御法を開発することにより歯髄保存に関する新しい知見を得られ炎症歯髄に対する新規治療の開発の端緒となると考えらえる。