| Project/Area Number |
10671030
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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 |
Endocrinology
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| Research Institution | The University of Tokyo |
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Principal Investigator |
TAKAHASHI Katsutoshi University of Tokyo, Fourth Department of Internal Medicine, Assistant Professor, 医学部・附属病院, 助手 (00292863)
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| Co-Investigator(Kenkyū-buntansha) |
ANDO Katsuyuki University of Tokyo, Department of Health Promotion Center, Lecturer, 保健管理センター, 講師 (60184313)
SHIMOSAWA Tastuo University of Tokyo, Fourth Department of Internal Medicine, Assistant Professor, 医学部・附属病院, 助手 (90231365)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,200,000 (Direct Cost: ¥3,200,000)
Fiscal Year 1999: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 1998: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | mitogen-activated protein kinase / vascular / atherosclerosis / advanced glycation end product / oxidized LDL / lnterleukin-8 / LOX-1 / filipin / マイクロドメイン / MAPkinese / AGE / IL-8 / LPS / MAP Kinase / 1L-8 |
|---|
| Research Abstract |
In both A10 VSMC and BAEC, osmotic stimulus, EGF, LPS potently activated p38MAPK. During its activation process, the involvement of cholesterol-rich microdomain(s) such as caveolae or raft was suggested by pharmacological experiments. As a potential molecular targets of p38MAPK in the vasculature, we focused on the lnterleukin-8 (IL-8) and the recently identified lectin-like oxidized LDL receptor-1 (LOX-1). We found advanced glycation end products (AGE) trigger IL-8 secretion in VSMC. Also, we found AGE upregulate LOX-1 gene expression in BAEC via redox-sensitive mechanism. However, the major role of p38MAPK was not suggested in these process. Further work is necessary to clarify the role of p38MAPK in the vascular function.
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