| Project/Area Number |
23592092
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | Ehime University |
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Principal Investigator |
KUMON YOSHIAKI 愛媛大学, 医学(系)研究科(研究院), 准教授 (80127894)
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| Co-Investigator(Kenkyū-buntansha) |
WATANABE Hideaki 愛媛大学, 大学院医学系研究科, 講師 (30322275)
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| Project Period (FY) |
2011 – 2013
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| Project Status |
Completed (Fiscal Year 2013)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 脳血管障害学 / BINCs / MCP-1 / Fractalkine / CCR2 / CX3CR1 / cerebral infarction / cerebral ischemia / microglia |
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| Research Abstract |
BINCs (Brain Iba1+/NG2+ Cells) accumulate in the ischemic core (IC), and may play neuroprotectively. The chemokine-based mechanisms underlying the invasion of BINCs were investigated.
We found isolated BINCs expressed mRNA encoding CCR2 and CX3CR1 at high levels. Cultured astrocytes expressed mRNA encoding their ligands, MCP-1 and fractalkine (FK). Recombinant MCP-1 and/or FK, as well as astrocytes, induced the migration of BINCs in vitro. The mRNA for MCP-1, FK, CCR2, and CX3CR1 was expressed in the IC during the acute phase. Immunohistochemical studies revealed vascular endothelial cells and astrocytic endfeet expressed MCP-1 and FK. CCR2+/Iba1+ monocytes attached to the inside of vascular wall at 1 day post-ischemia (dpi), and there were CCR2+/CX3CR1+ macrophage-like cells in the parenchyma of the IC at 2 dpi, which may be progenitors for BINCs. These results suggest CCR2+ monocytes are first attracted to the IC by MCP-1+ endothelial cells and migrate toward FK+ astrocytic endfeet.
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