| Project/Area Number |
20590567
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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 | Kyoto University |
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Principal Investigator |
IKEMOTO Masaki Kyoto University, 大学院・医学研究科, 准教授 (80144385)
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| Co-Investigator(Kenkyū-buntansha) |
UEMOTO Shinji 京都大学, 大学院・医学研究科, 教授 (40252449)
EGAWA Haruto 朝日大学, 歯学部, 教授 (40293865)
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| Project Period (FY) |
2008 – 2010
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| Project Status |
Completed (Fiscal Year 2010)
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| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2010: ¥780,000 (Direct Cost: ¥600,000、Indirect Cost: ¥180,000)
Fiscal Year 2009: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2008: ¥2,730,000 (Direct Cost: ¥2,100,000、Indirect Cost: ¥630,000)
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| Keywords | S100蛋白 / マクロファージ / 好中球 / 拒絶反応 / 急性炎症 / サイトカイン / S100A8/A9 / フィブロネクチン / アンチトロンビンIII / プラスミノーゲン / S100A8 / A9 / Neutrophils / Macrophages / Cytokines / Acute inflammation / Inflammatory marker / Lipopolysaccharide / Liver damage / Neutrophil / Macrophage |
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| Research Abstract |
We found that S100A8/A9 non-specifically bind with fibronectin (h-FN), and that both the two protein exist on surface membrane of neutrophils and monocytes. The h-FN could be conclusively transported with S100A8/A9 in blood and/or on immunological cells, and effectively prevent further attack by various internal oxidants or repair damaged liver tissue in vivo. When recombinant human S100A8 was intravenously injected in the rats with LPS-induced liver damage, not only expression of r-S100A9 but also the activities of AST, ALT and LD significantly went down in comparison with those of the rats with liver damage, strongly suggested that the r-S100A8 could serve as a regulator of acute inflammatory reaction in the rats with LPS-induced damage. Immunohistochemistry provided interesting microscopic images, in which much r-S100A8 and r-S100A9 were observed in many macrophages in the heart tissues of rats with experimental autoimmune myocarditis. In addition, macrophages were positive for not only CD68 antigen but also r-S100A8 and/or r-S100A9 proteins, strongly suggesting active condition of the macrophages in inflamed areas of the heart tissues with EAM. Therefore, r-S100A8 and r-S100A9 in macrophages should be novel indexes for active condition of the cells in the EAM rats.
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