| Project/Area Number |
13671448
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Cerebral neurosurgery
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| Research Institution | OITA MEDICAL UNIVERSITY |
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Principal Investigator |
ISONO Mitsuo Oita University, School of Medicine, Assistant Professor, 医学部, 助教授 (60151437)
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| Co-Investigator(Kenkyū-buntansha) |
KAMIDA Tohru Oita University, School of Medicine, Associate Professor, 医学部, 講師 (90315333)
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| Project Period (FY) |
2001 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥2,500,000 (Direct Cost: ¥2,500,000)
Fiscal Year 2002: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2001: ¥1,100,000 (Direct Cost: ¥1,100,000)
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| Keywords | TGF / astrocyte / microglia / BrDU / TGF2 / astrogliosis / IL-6 |
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| Research Abstract |
To determine the exact role of TGF-α in glial activation after traumatic brain injury, we investigated the astroglial and microglial responses after cortical stab wound injury in TGF-α overexpressing mice. Adult male B6D2-TgN (MMTVTGFA) 29RjC transgenic mice were used for the subjects. This transgenic line carries a TGF-alpha cDNA under the control of the dexamethasone-inducible MMTV promoter. Thus, exogenous administration of dexamethasone induces TGF-α overexpression. Male B6D2F1/J mice at the same age served as wild-type animals. After the cortical stab wound injury, expression of glial fibrilary acidic protein, CD-11b and interleukine-6 were investigated immunohistochemically. The results indicate that TGF-α might affect astrocytic hypertrophy without affecting microgliosis not only in the normal condition, but also in the pathological condition. Moreover, overexpression of TGF-α induced obvious expression of IL-6 around the lesion. This fact might indicate possible role of TGF-α in affecting neuronal function.
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