Project/Area Number |
21700402
|
Research Category |
Grant-in-Aid for Young Scientists (B)
|
Allocation Type | Single-year Grants |
Research Field |
Neurochemistry/Neuropharmacology
|
Research Institution | University of Fukui |
Principal Investigator |
IGUCHI Tokuichi University of Fukui, 医学部, 特命助教 (60509305)
|
Project Period (FY) |
2009 – 2010
|
Project Status |
Completed (Fiscal Year 2010)
|
Budget Amount *help |
¥4,420,000 (Direct Cost: ¥3,400,000、Indirect Cost: ¥1,020,000)
Fiscal Year 2010: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2009: ¥2,990,000 (Direct Cost: ¥2,300,000、Indirect Cost: ¥690,000)
|
Keywords | 神経科学 / 細胞・組織 / シグナル伝達 / サイトカイン / 神経新生 / 脳梗塞 / 細胞死 / 大脳皮質 |
Research Abstract |
It is known that neurogenesis happens at the region of the injuries such as the stroke, and the elucidation of the mechanism leading from the death to the regeneration of the cell has high therapeutic implications. We found that EMAP-II, a molecule secreted owing to cell death, was increased in peripheral blood vessels during a stroke. Furthermore, EMAP-II acted on neural stem cells to induce the expression of FILIP1L which participats in proliferation and differentiation of a cell. Both of them were highly expressed in the olfactory bulb where the neurogenesis occurs actively. These results suggested a part of the mechanism linking cell death and neurogenesis.
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