| Project/Area Number |
09670663
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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 | Nagoya City University |
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Principal Investigator |
ITO Jinchi Nagoya City University, Biochemistry, assistant professor, 医学部, 講師 (60167260)
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| Co-Investigator(Kenkyū-buntansha) |
YOKOYAMA Shingi Nagoya City University, Biochemistry, professor, 医学部, 教授 (10142192)
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| Project Period (FY) |
1997 – 1998
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| Project Status |
Completed (Fiscal Year 1998)
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| Budget Amount *help |
¥2,900,000 (Direct Cost: ¥2,900,000)
Fiscal Year 1998: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1997: ¥1,900,000 (Direct Cost: ¥1,900,000)
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| Keywords | astrocyte / apolipoprotein E / apo AI / cholesterol / HDL / ホスファチジルコリン / LDL |
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| Research Abstract |
Central nervous system (CNS) is under the environment to be difficult to deliver and accept cholesterol through the interaction with lipoproteins in blood. In order to understand the function of astrocytes to regulate cholesterol metabolism of CNS, the mechanism of cholesterol efflux and influx of astrocytes were investigated. Rat astrocytes secreted apoE and generate extracellularly cholesterol-rich HDL with cholesrol and phospholipid, and produced separately cholesterol-poor HDL dependent on exogeouns apoAl. Two kinds of HDL produced by astrocytes were considered to relate to cholesterol transport between cells in brain. It was suggested that HDLs were produced by endogenous apoE and exogenous apoAl through different mechanism, respectively, The extracellular apoE secreted by rat astrocytes was recovered from HDL fraction by sucrose-density ultracentrifugation, although it was done partly from high density protein fraction. Cyclosporin A, a inhibitor of calcineulin, suppressed apoAl-induced cholesterol efflux but not endogenous apoE-dependent one. These findings suggest that apoE is secreted as cholesterol-bound type but not as cholesterol-free type by astrocytes.
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