| Project/Area Number |
08457258
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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 |
内分泌・代謝学
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| Research Institution | Research Center for Advanced Science and Technology University of Tokyo |
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Principal Investigator |
KODAMA Tatsuhiko University Tokyo, , Research Center for Advanced and Technology, Chair Professor, 先端科学技術研究センター, 教授 (90170266)
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| Co-Investigator(Kenkyū-buntansha) |
WADA Youithirou Japan Foundation for Aging and Health, Research Resident, リサーチレジデント
NAKAZIMA Atsushi University of Tokyo, , The Third Department of Internal Medicine, Assistant Prof, 医学部・第三内科, 助手
ABURATANI Hiroyuki University of Tokyo, , The Third Department of Internal Medicine, Assistant Prof, 医学部・第三内科, 助手 (10202657)
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| Project Period (FY) |
1996 – 1997
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| Project Status |
Completed (Fiscal Year 1997)
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| Budget Amount *help |
¥8,800,000 (Direct Cost: ¥8,800,000)
Fiscal Year 1997: ¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1996: ¥5,200,000 (Direct Cost: ¥5,200,000)
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| Keywords | macrophage / scavenger receptor / knockout mice / foam cell / atherosclerosis / スフェロプラストフュージョン / ノックアウトマウス / マクロファージ / コレステロール / 動脈硬化 / 酸素ラジカル |
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| Research Abstract |
Macrophage type-I and type-II class-A scavenger receptors (MSR-A) are implicated in the pathological deposition of cholesterol during atherogenesis as a result of receptor-mediated uptake of modified low-density lipoprotains (mLDL). MSR-A can bind an extraordinarily wide range of ligands, including bacterial pathogens, and also mediates cation-independent macrophage adhesion in vitro. Herer we show that targeted disruption of the MSR-A gene in mice results in a reduction in the size of atherosclerotic lesions in an animal deficient in apolipoprotein E.Macrophages from MSR-A-deficient mice show a marked decrease in mLDL uptake in vitro, whereas mLDL clearance from plasma occurs at a normal rate, indicating that there may be alternative mechanisms for removing mLDL from the circulation.In addition, MSR-A-knockout mice show an increased susceptibility to infection with Listeria monocytogenes or herpes simplex virus type-1, indicating that MSR-A may play a part in host defense against pathogens.
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