| Project/Area Number |
25860164
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
General physiology
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| Research Institution | Kobe University |
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Principal Investigator |
ENDO Mitsuharu 神戸大学, 医学(系)研究科(研究院), 助教 (90436444)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,160,000 (Direct Cost: ¥3,200,000、Indirect Cost: ¥960,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | Ror1 / Ror2 / Wnt5a / アストロサイト / 脳損傷 / bFGF / 増殖 / 細胞周期 / Ror / 炎症 |
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| Outline of Final Research Achievements |
The Ror-family receptor tyrosine kinases, Ror1 and Ror2, have been shown to act as receptors for Wnt5a and paly essential roles during development. We found that Ror1 and Ror2 are induced in the adult mouse brain following injury. Immunohistochemical analysis using the anti-Ror2 antibody revealed that Ror2 was up-regulated on reactive astrocytes around the lesion site, although Ror1-expressing cells within injured brain regions could not be identified due to lack of a usable anti-mouse Ror1 antibody for immunostaining. We also found that Ror2 was induced upon stimulation with bFGF in cultured astrocytes, and up-regulation of Ror2 was required for bFGF-induced cell cycle re-entry of quiescent astrocytes. These findings indicate that bFGF-induced expression of Ror2 plays an important role in regulating proliferation of reactive astrocytes following brain injury.
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