Cyclopedic analysis of microglia at the cerebral infarction : The dynamics and treatment application
Project/Area Number |
18K16587
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Research Category |
Grant-in-Aid for Early-Career Scientists
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Allocation Type | Multi-year Fund |
Review Section |
Basic Section 56010:Neurosurgery-related
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Research Institution | Ehime University |
Principal Investigator |
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Project Period (FY) |
2018-04-01 – 2020-03-31
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Project Status |
Completed (Fiscal Year 2019)
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Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2019: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2018: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
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Keywords | 脳虚血 / マイクログリア / アポトーシス / 貪食 / Eat-me signal / 脳梗塞 / eat-me signal / TGF-β1 |
Outline of Final Research Achievements |
Activated microglia phagocytose neurons which survived at the periphery of cerebral infarction through eat-me signal cascade; ProteinS/MerTK and complement/CD11b. This Phagocytosis is thought to be associated with delayed neuronal loss (DNL). GM-CSF/IL-3 increased expression of the anti-apoptotic molecule Bcl-xL on neurons. The Bcl-xL maintained the mitochondrial function of neurons and increased the intracellular ATP. The intracellular ATP decreased phosphatidylserine which was exposed to the neuronal surface , eat-me signal molecules was less likely to combine with neurons, and neuronal phagocytosis by the microglia was suppressed.
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Academic Significance and Societal Importance of the Research Achievements |
重症脳梗塞は、虚血超急性期の後も徐々に神経細胞死が進行していくことが臨床上重要な問題である。虚血辺縁部では、生存した神経細胞がマイクログリアによって貪食されている現象が起こっている。本研究では、この神経細胞とマイクログリアの貪食に関わっているeat-me signalの分子を解明した。また、GM-CSF/IL-3というサイトカインが、この虚血辺縁の神経細胞のアポトーシス、マイクログリアの貪食を抑制する作用があることを示し、脳梗塞治療ターゲットとなりうる可能性があることを示した。
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Report
(3 results)
Research Products
(6 results)
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[Journal Article] Comparison of the detrimental features of microglia and infiltrated macrophages in traumatic brain injury: a study using a hypnotic bromovalerylurea2018
Author(s)
Abe N, Choudhury ME, Watanabe M, Kawasaki S, Nishihara T, Yano H, Matsumoto S, Kunieda T, Kumon Y, Yorozuya T, Tanaka J
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Journal Title
Glia
Volume: 66(10)
Issue: 10
Pages: 2158-2173
DOI
Related Report
Peer Reviewed / Open Access
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