2002 Fiscal Year Final Research Report Summary
ROLE OF FOAM CALL DEATH ON ATHEROSCLEROSIS
| Project/Area Number |
13672427
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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 |
Laboratory medicine
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| Research Institution | Jichi Medical School |
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Principal Investigator |
KUBO Nobuhiko Jichi Medical School, Dpt. of Medicine, Assistant Professor, 医学部, 講師 (40214994)
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| Co-Investigator(Kenkyū-buntansha) |
KANNO Hiroshi Yokohama City University, Dpt. of Medicine, Assistant Professor, 医学部, 講師 (40244496)
YAMADA Shigeki Jichi Medical School, Dpt. of Medicine, Assistant Professor, 医学部, 講師 (80220375)
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| Project Period (FY) |
2001 – 2002
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| Keywords | AHTEROSCLESOSIS / APOPTOSIS / MACROPHAGE / FOAM CELL / FAS / SMOOTH MUSCLE CELLS |
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| Research Abstract |
The aims of this study are to examine the connection between apoptosis with related molecules and lesion morphology as well as stability of human atherosclerotic tissues obtained by endoatherectomy. Macrophage foam cell apoptosis was investigated in foam cells of multiple human cartoid atherosclerotic tissues obtained by endoatherecotmy. Apoptosis in human atherosclerotic tissues were rare event however, the cell death was highest in areas adjacent to the lipid core whrere there was relatively thin layer of connective tissue, a feature that is characteristic of unstable lesion than in other areas of foam cell accumulation. We further investigated role of macrophage-specific Fas in the LDLR-/-mice. Bone marrow cells of LDLR-/-mice were reproduced with marrow from either Fas-deficient lpr (lpr-BMT) or wild-type (WT-BMT) mice. The connective tissue fibrous cap was much thinner and the lipid core was more prominent in the lesions of lpr-BMT mice. The lpr-BMT mice had considerably less TUNEL-positive staining throughout the lesion as compared to the WT-BMT mice. Our conclusions are that macrophages in human carotid atherosclerotic lesion may partly be protected from cell death by expressing apoptosiss inhibitory molecules, and a role of macrophages cell death through Fas on the lesion stability was indicated.
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