| Project/Area Number |
11480226
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Nerve anatomy/Neuropathology
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| Research Institution | Osaka University |
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Principal Investigator |
UCHIYAMA Yasuo Osaka University Graduate School of Medicine, Department of Cell Biology and Neuroscience, Professor, 医学系研究科, 教授 (10049091)
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| Co-Investigator(Kenkyū-buntansha) |
ISHIHARA Kyoko Osaka University Graduate School of Medicine, Department of Cell Biology and Neuroscience, Assistant Professor, 医学系研究科, 助手 (30303944)
OHSAWA Yoshiyuki Osaka University Graduate School of Medicine, Department of Cell Biology and Neuroscience, Assistant Professor, 医学系研究科, 助手 (30273642)
WAGURI Satoshi Osaka University Graduate School of Medicine, Department of Cell Biology and Neuroscience, Associate Professor, 医学系研究科, 助教授 (30244908)
KAMETAKA Satoshi Osaka University Graduate School of Medicine, Department of Cell Biology and Neuroscience, Assistant Professor, 医学系研究科, 助手 (10303950)
渡部 剛 大阪大学, 医学系研究科, 助教授 (80220903)
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| Project Period (FY) |
1999 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥14,900,000 (Direct Cost: ¥14,900,000)
Fiscal Year 2001: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 2000: ¥2,800,000 (Direct Cost: ¥2,800,000)
Fiscal Year 1999: ¥9,300,000 (Direct Cost: ¥9,300,000)
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| Keywords | PCTF35 / Brain injuries / Astrocytes / Glyosis / TGF-b1 / Primary culture / Induction / Secretion / TGFB1 / 栄養因子 / 低酸素虚血障害 / 海馬CA1領域 / 錐体神経細胞 / ラット新生仔 / 神経栄養因子 / PC12細胞 / bcl-2 / 脊髄後根神経節 / 神経細胞死 / 神経突起 / NGF |
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| Research Abstract |
To understand in vivo functions of PCTF35, we performed the following experiments using models of brain injuries and primary cultured astrocytes.
1) Expression of PCTF35 following brain injuries: For this we prepared the following two animals; (1) Hypoxia-ischemia (H-1) injury: new born rats at P7 were anesthetized and the left common carotid artery was ligated. The animals were returned to the darn for 1 hr and then placed in containers, which were perfused with mixed gases of 8% oxygen and 92% nitrogen and kept at 37℃, for 90 min. They were then returned to the dam until used. (2) Penetrating brain injury: Adult rats (8 weeks of age) were anesthetized and an incision with a 2mm depth and 4mm length was made in the temporal lobe after part of the temporal bone was opened. These animals were perfused from the heart with 4% paraformaldehy, de 3,4,5 and 7 days after the operation and brain tissues were processed for immunohistochemistry. At 3 days, GFAP-immunopositive astrocytes expanded their process and invaded into injured areas, while astogliosis occurred in the areas at 7 days. By double immunostaining, immunoreactivity for PCTF35 from co-localized in the processed of these astrocytes with that for GFAP.
2) Expression and secretion of PCTF35 from primary cultured astrocytes: Since PCTF35 was induced in astrocytes appearing in injured areas of brains, we separated astrocytes from brains of rats at P2. PCTF35 was found in the cultured medium of primary astrocytes by Western blot and the amount of the protein was significantly increased in the medium when TGF-β1 was added in cultures. These lines of evidence suggest that PCTF35 is induced in astrocytes of rat brains after H-I and penetrating injuries and this induction is enhanced by TGF-β1.
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