| Project/Area Number |
17H06757
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| Research Category |
Grant-in-Aid for Research Activity Start-up
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| Allocation Type | Single-year Grants |
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| Research Field |
Surgical dentistry
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| Research Institution | Nagoya University |
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Principal Investigator |
Kano Fumiya 名古屋大学, 医学部附属病院, 医員 (40801626)
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| Project Period (FY) |
2017-08-25 – 2019-03-31
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| Project Status |
Completed (Fiscal Year 2018)
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| Budget Amount *help |
¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
Fiscal Year 2018: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Keywords | 神経障害性疼痛 / ミクログリア / エクソソーム / MCP-1 / Siglec / マクロファージ / 歯髄幹細胞 / Siglec-9 / 帯状疱疹 / 神経変性 / M2マクロファージ / 疼痛 |
|---|
| Outline of Final Research Achievements |
"Pain" is an important sense that informs the body of the invasion and damage, but there is "neuropathic pain" that persists even if the damage is repaired. It is known that the inflammation is degeneration of microglia. By applying anti-inflammatory M2 microglia-inducing factor to neuropathic model mice, the applicant transforms the tissue destructive inflammatory response into anti-inflammatory / tissue regeneration type Was found to promote pain control. In addition, the induced endoplasmic reticulum (exosome) released by M2 microglia was taken into the surrounding Schwann cells to control pain by controlling the inflammatory state and suppressing cell death.
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| Academic Significance and Societal Importance of the Research Achievements |
疼痛の慢性化するメカニズムとして、神経細胞だけでなく、損傷した末梢神経に浸潤・集積するマクロファージと脊髄後角で活性化するミクログリアが重要な役割を担うことを示す基礎的論文が数多く蓄積されている。本研究はミクログリアやマクロファージの役割を深めることで、慢性疼痛のメカニズムの解明と治療薬の開発につながる重要な研究と考える。
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