2020 Fiscal Year Final Research Report
Elucidation of mechanism of neurovascular unit remodeling in repair model after stroke
| Project/Area Number |
18K15035
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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 48030:Pharmacology-related
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| Research Institution | Kindai University |
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Principal Investigator |
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| Project Period (FY) |
2018-04-01 – 2021-03-31
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| Keywords | 脳卒中 / neurovascular unit / 血管内皮細胞 / マクロファージ / 終末糖化産物 / 血管新生 / HMGB1 / 血小板 |
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| Outline of Final Research Achievements |
In stroke-prone spontaneously hypertensive rat (SHRSP), we investigated the change of HMGB1, representative DAMPs and regenerative mediator, and the involvement of HMGB1 on angiogenesis. The decreased HMGB1 levels was observed in infarct area and serum after development of stroke. The increased volume of platelet, which one of source for HMGB1, were observed at 3 weeks before development of stroke. In addition, the decreased lymphocytes count was observed at 3 weeks before development of stroke. Although HMGB1 has no pro-angiogenic activity, advanced glycation end products, which activate same receptors with HMGB1, facilitated angiogenesis.
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| Free Research Field |
血管、再生
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| Academic Significance and Societal Importance of the Research Achievements |
脳卒中発症に至る過程におけるHMGB1の挙動に関する知見を得た。脳卒中を自然発症するモデル動物の特性を生かし、HMGB1の供給源として検討を進めた血球系の解析において、脳卒中発症前の変動をとらえることができた。血小板の大型化とリンパ球の低下は脳卒中の発症を事前に予測するために有用な特徴であり、バイオマーカーとして利用できる可能性がある。これらのパラメーターは簡便でかつ低コストで測定可能であるため、今後、臨床研究への応用が期待できる。
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