1996 Fiscal Year Final Research Report Summary
action of apolipoprotein E on cultured neuronal cells
| Project/Area Number |
07670705
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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 |
Neurology
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| Research Institution | Fukui Medical School |
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Principal Investigator |
HIRAYAMA Mikio Fukui Medical School, Dept.Medicine, Associate Professor, 医学部, 助教授 (30181192)
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| Co-Investigator(Kenkyū-buntansha) |
ITO Keita Fukui Medical School, Dept.Medicine, Associate, 医学部, 助手 (40273007)
KURIYAMA Masaru Fukui Medical School, Dept.Medicine, Professor, 医学部, 教授 (80107870)
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| Project Period (FY) |
1995 – 1996
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| Keywords | apolipoprotein E / microglia / astrocyte / cytokine / LDL receptor / scavenger receptor / TGF-beta / IL-1-beta |
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| Research Abstract |
Binding of acetylated LDL was strongly observed in rat microglia, while mild binding was observed in oligodendrocytes, O-2A progenitor cells and type 2 astrocytes. There was no binding to type 1 astrocytes. The presence of scavenger receptor was indicated in microglia. Binding of LDL to oligodendrocytes and O-2A progenitor cells was observed and indicates the active metabolism of lipids. Further study is necessary for the regulation of scavenger receptor in relation to cytokine, amyloid and apolipoprotein E.
We examined the effect of cytokine on the regulation of the expression of apoE mRNA of astrocytes and microglia from new-born mouse brain. ApoE mRNA expression was assessed by RT-PCR method. Microglia ; GM-CSF,TGF-beta upregulated the expression of apoE mRNA in 1 day. IL-1-beta downregulated the expression of apoE mRNA.Astrocyte : In control astrocytes, there was no detection of apoE mRNA.TGF-beta upregulated for 1 day, IL-1-beta upregulated the expression of apoE mRNA after 3 days. The regulation of apoE mRNA in microglia might be caused by astrocytes that produce GM-CSF,TGF-beta, Il-l-beta. The interrelationship of each cytokine should be studied. The regulation of apo E mRNA in astrocytes was observed by TGF-beta, thus indicating the possibility of the involvement in pathogenesis of Alzheimer's disease.
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