| Project/Area Number |
12835007
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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 Institution | Kobe University |
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Principal Investigator |
HIRATA Ken-ichi Kobe University, Hospital, Assistant Professor, 医学部・附属病院, 講師 (20283880)
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| Co-Investigator(Kenkyū-buntansha) |
INOUE Nobutaka Kobe University, Graduate School of Medicine, Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Assistant Professor, 大学院・医学系研究科, 助手 (10304099)
YOKOYAMA Mitsuhiro Kobe University, Graduate School of Medicine, Division of Cardiovascular and Respiratory Medicine, Department of Internal Medicine, Professor, 大学院・医学系研究科, 教授 (40135794)
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| Project Period (FY) |
2000 – 2001
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| Project Status |
Completed (Fiscal Year 2001)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2001: ¥1,500,000 (Direct Cost: ¥1,500,000)
Fiscal Year 2000: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | lipase / lipoprotein / atherosclerosis / endothelial cell / smooth muscle cell / macrophage / coronary artery / molecular cloning / 血管内皮細胞 / HDL / 免疫組織化学 |
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| Research Abstract |
Recently, we have cloned endothelial cell-derived lipase (EDL), a new member of the lipase gene family',' from endothelial cells during vascular formation. To investigate local control of lipase activity in the blood vessel wall, we examined the regulation of EDL expression in cultured human umbilical vein and coronary arterial endothelial cells. EDL mRNA was upregulated in.endothelial cells by inflammatory.cytokines implicated in vascular disease etiology, including TNF-αand IL-1β. In addition, cyclic strairi and fluid shear stress also upregulated the mRNA expression of EDL. Next, we cloned rat EDL (rEDL) cDNA from cultured vascular smooth muscle cells (VSMC). rEDL mRNA expression was also upregulated by Ang II. The presence of LPL in the vascular wall has been implicated in the progression of atherosclerosis. The aim of this study was to investigate the local expression of EDL in human coronary arteries. Immunohistochemical analysis revealed that EDL was expressed in endothelial cells and medial smooth muscle cells in non-atherosclerotic coronary arteries. In addition, EDL was detected in endothelial and smooth muscle cells, as well as infiltrating cells, in the atheromatous plaque. Taken together presence of EDL and regulated expression of EDL may have unique functional roles in the pathogenesis of coronary artery diseases such as atherosclerosis as well as in lipid metabolism in the vessel wall.
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