| Project/Area Number |
16380211
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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 |
Clinical veterinary science
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| Research Institution | The University of Tokyo |
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Principal Investigator |
MATSUKI Naoaki The University of Tokyo, Graduate School of Agricultural and Life Sciences, Associate Professor, 大学院・農学生命科学研究科, 助教授 (40251417)
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| Co-Investigator(Kenkyū-buntansha) |
ONO Kenichiro The University of Tokyo, Graduate School of Agricultural and Life Sciences, Professor, 大学院・農学生命科学研究科, 教授 (50111480)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥9,900,000 (Direct Cost: ¥9,900,000)
Fiscal Year 2005: ¥3,800,000 (Direct Cost: ¥3,800,000)
Fiscal Year 2004: ¥6,100,000 (Direct Cost: ¥6,100,000)
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| Keywords | Dogs / Autoimmunity / Necrotizing meningoencephalitis / Granulomatous meningoencephalitis / GFAP / Glutamate / EAAT / 自己抗体 / グリア線維性酸性蛋白質 / クローニング |
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| Research Abstract |
1)GFAP is a common autoantigen in canine necrotizing nemingoencephalitis and granulomatous meningoencephalitis : To identify the common autoantigen(s) in canine idiopathic encephalitis, we collected cerebrospinal fluids from 40 dogs with necrotizing meningoencephalitis (NME) or granulomatous meningoencephalitis (GME). Eighty dogs with other CNS diseases were also examined. By Western blotting on canine brain proteins and MALDI-TOF-MASS, glial fibrillaly acidic protein (GFAP) was the candidate of autoantigen. In fact patients' CSFs reacted with purified bovine GFAP. These results clearly showed that GFAP is a common autoantigen in canine NME as well as in GME.
2)CSFs from NME dogs inhibit glutamate uptake into normal canine astrocytes : To clarify the effect of NME or GME to glutamate homeostasis in the brain, cultured canine astrocytes were treated with CSFs from NME (GME) patients. Glutamate concentrations in the supernatants were elevated in the treated cultures, with the significant decrease in mRNAs of glutamate transporters (EAAT1 and 2). Thus, NME and GME inhibit glial glutamate uptake, which can lead to neuronal damage in the brain.
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