2003 Fiscal Year Final Research Report Summary
Regulation of ACAT in multiple risk factor syndrome
| Project/Area Number |
14571101
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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 |
Metabolomics
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| Research Institution | Showa University |
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Principal Investigator |
MIYAZAKI Akira Showa University School of Medicine, Department of Biochemistry, Professor, 医学部, 教授 (70253721)
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| Co-Investigator(Kenkyū-buntansha) |
HAGIWARA Tamio Showa University School of Medicine, Department of Biochemistry, Associate Professor, 医学部, 講師 (50228392)
IWAMOTO Sanju Showa University School of Medicine, Department of Biochemistry, Associate Professor, 医学部, 講師 (50176567)
HONGO Shigeki Showa University School of Medicine, Department of Biochemistry, Associate Professor, 医学部, 講師 (40054043)
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| Project Period (FY) |
2002 – 2003
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| Keywords | ACAT / ACAT2 / macrophage / atherosclerosis / foam cell / differentiation |
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| Research Abstract |
Acyl-coenzyme A: cholesterol acyltransferase 1 (ACAT1) was regarded as a major ACAT isoform expressed in human macrophages. However, the current immunohistochemical studies with an ACAT2 antibody demonstrated significant expression of ACAT2 in macrophage-foam cells in human atherosclerotic lesions. All the macrophages in the lesions expressed ACAT1 while 70-80% of the macrophages expressed ACAT2. Immunoblot and RT-PCR analyses of cultured human monocyte-macrophages demonstrated that immature macrophages expressed only ACAT1 while fully differentiated macrophages expressed both ACAT1 and ACAT2. Additional immunoblot and RT-PCR analyses showed that mouse peritoneal exudate macrophages expressed both ACAT1 and ACAT2 while mouse resident peritoneal macrophages expressed only ACAT1. We conclude that under various pathological conditions, fully differentiated macrophages express ACAT2 in addition to ACAT1.
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