| Project/Area Number |
13671061
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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 |
Hematology
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| Research Institution | KYOTO UNIVERSITY |
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Principal Investigator |
SASADA Masataka Kyoto University, Medical Technology, Professor, 医療技術短期大学部, 教授 (30144364)
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| Project Period (FY) |
2001 – 2002
|
| Project Status |
Completed (Fiscal Year 2002)
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| Budget Amount *help |
¥3,100,000 (Direct Cost: ¥3,100,000)
Fiscal Year 2002: ¥1,300,000 (Direct Cost: ¥1,300,000)
Fiscal Year 2001: ¥1,800,000 (Direct Cost: ¥1,800,000)
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| Keywords | nitric oxide / endothel / guanylate cyclase / transmigration / neutrophils / 遊走 / トランスミグレーション / 血管内皮 |
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| Research Abstract |
Neutrophils are generated in the bone marrow and released into blood stream. Then, they pass through endothelial cells and move into tissues. Since neutrophils function in host defense mainly in the tissue, transendothelial migration (TEM) is important in the aspect that the number of neutrophils in the tissue is modulated by TEM. Nitric oxide (NO) has been reported to be generated by endothelial cells and affect on the adhesion of neutrophils to endothelial cells, although there are some conflicting reports. Our aim of this research project is to clarify the role of NO on TEM of neutrophils. Followings are the findings and results of this research project.
NO inhibits neutrophil TEM.
Supplementation of exogenous NO inhibited neutrophil TEM.
NO synthase inhibitor and NO quencher increased TEM of neutrophils.
NO is produced by endothelial cells.
NO quencher increased TEM of neutrophils.
NO synthase inhibitor increased TEM of neutrophils.
NO was detected in endothelial cells.
NO acts on neutrophils.
NO was detected in neutrophils after neutrophils were co-cultured with endothelial cells.
NO activates guanylate cyclase and modulates TEM of neutrophils.
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