2022 Fiscal Year Final Research Report
The effects of HMGB1 produced by vascular endothelial cells in periodontal tissue on systemic diseases.
| Project/Area Number |
20K18535
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| Research Category |
Grant-in-Aid for Early-Career Scientists
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| Allocation Type | Multi-year Fund |
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| Review Section |
Basic Section 57030:Conservative dentistry-related
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| Research Institution | Okayama University |
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Principal Investigator |
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| Project Period (FY) |
2020-04-01 – 2023-03-31
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| Keywords | 低栄養 / HMGB1 / 創傷治癒 / 幹細胞 |
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| Outline of Final Research Achievements |
HMGB1 induces an inflammatory response, an essential response to initiate wound healing via RAGE. We hypothesized that malnutrition may interfere with this cascade, leading to abnormal inflammation and ultimately delaying wound healing. At 3 and 7 days after tooth extraction, we histologically examined wound tissue and analyzed several factors of the inflammatory-regenerative lineage. 7 days later, under malnutrition, mRNA expression of genes for regeneration and mesenchymal stem cell (MSC) accumulation decreased and mRNA expression of myeloperoxidase and IL-1β clearly increased, delayed wound healing with findings such as increased HMGB1 levels and increased ATP concentrations in tissues with an increased percentage of M2 macrophages.
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| Free Research Field |
歯周病態学分野
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| Academic Significance and Societal Importance of the Research Achievements |
近年ではHMGB1が組織修復にも関与することが報告されてきた。本研究では，栄養失調状態下でのATP産生およびRAGE経路を介したIL-1β分泌の上昇に伴うHMGB1分泌量の著しい増加が、炎症や創傷治癒を阻害する可能性に関わることが明らかとなった。
栄養不良の個体における創傷治癒の遅延のメカニズムに関する研究は、栄養不良に関連する短期的な疾患を目標に促進または抑制するための新しい視点を提供する可能性がある。歯周組織由来の HMGB1 が全身疾患に関与していることが明らかとなれば，HMGB1 をターゲットとした新規の全身疾患の治療法が確立される可能性が考えられる。
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