| Project/Area Number |
12670218
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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 |
Experimental pathology
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| Research Institution | Soka University |
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Principal Investigator |
WATANABE Rihito Soka University, Institute of Life Science, Professor, 生命科学研究所, 教授 (30129746)
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| Co-Investigator(Kenkyū-buntansha) |
FUKUMITSU Hidehumi , 助手 (00308280)
NAKAJIMA Kazuyuki , 講師 (50175494)
TAKASE Sayaka , 助教授 (60236221)
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| Project Period (FY) |
2000 – 2002
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| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2002: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 2001: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2000: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | Retorovirus / microglia / Neuropathogenic / ecotropic / retroviral vector / tissue culture / recombinant virus / spongiosis |
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| Research Abstract |
During the first year of the project, we established the optimal condition for the culture of microglial cells derived from new-born rat brain. When the 100,000 MW biglican-like haematopoietic factor (BHF) was added to the microglial culture medium, the growth of microglia was increased by ten times of the culture without BHF. However, the infectivities of retroviruses to the microglia were almost diminished in the culture with BHF.
Retroviral vector carring LacZ genom that was constructed in our laboratory based on A8-V genom (See the publication list), was infected to the cultured microglia. Nearly 100% of the cultured microglia were found to be labeled by LacZ after the infection. Those labeled microglia were injected into the new-born rat brain. Most of the transplanted and labeled microglia were found in the sub-arachnoidal space or in the perivascular space in the brain. Next, microglia infected with A8-V were injected into the new-born rat brain. We expected the enhanced lesion characterized by spongiotic degeneration in the brain after the injection compared with direct infection of the A8-V into the brain. However, the lesions induced by the infected microglia were of minimum degree. In addition, the lesions disappeared after 8 months of the implantation of the infected microglia whereas the rats that received the direct A8-V infection, exhibited wide-spread spongiotic degeneration in the brain 8 months after the infection and died at this stage.
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