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2023 Fiscal Year Final Research Report

Protection of pancreatic beta cell function and prevention of diabetic periodontitis by exosomes from human gingiva-derived MSCs.

Research Project

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Project/Area Number 22K21064
Research Category

Grant-in-Aid for Research Activity Start-up

Allocation TypeMulti-year Fund
Review Section 0907:Oral science and related fields
Research InstitutionKyushu University

Principal Investigator

Nishimura Yuki  九州大学, 歯学研究院, 助教 (40961925)

Project Period (FY) 2022-08-31 – 2024-03-31
Keywords歯肉幹細胞由来エクソソーム / 膵β細胞機能 / 糖尿病性歯周炎
Outline of Final Research Achievements

First, we stimulated mouse pancreatic β-cells (βTC6) with palmitic acid (PA), a saturated fatty acid, and analyzed Xaf1 expression in the PA alone stimulation group (PA group) and in the PA+Exo group, in which human gingival stem cell-derived exosomes (Exo) were added. The results showed that there was no significant difference in Xaf1 expression between the PA and PA+Exo groups in pancreatic β-cells (βTC6).
Second, we performed the same PA stimulation on mouse macrophages (RAW264.7) and analyzed Ifnβ expression in the PA and PA+Exo groups. The results showed that Ifnβ expression was significantly attenuated in mouse macrophages (RAW264.7) in the PA+Exo group compared to the PA group.

Free Research Field

歯周病学

Academic Significance and Societal Importance of the Research Achievements

ヒト歯肉幹細胞由来エクソソームの抗炎症作用は、in vitroにおいてマウスマクロファージ(RAW264.7)で選択的に確認されることを確認した。これを受け、in vivoにおいてもマクロファージを介したエクソソームの抗炎症効果が期待できるとの仮説を得た。すなわち、ヒト歯肉幹細胞由来エクソソームは直接的に膵β細胞のアポトーシス抑制に関与しないが、マクロファージを介する抗炎症効果によって間接的に膵β細胞のアポトーシスを抑制すると考えられる。この研究により、将来的にはエクソソームのマクロファージを介した抗炎症効果による糖尿病および歯周病双方の進展抑制を目指した治療薬開発が期待できる。

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Published: 2025-01-30  

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