| Project/Area Number |
16590252
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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 |
Pathological medical chemistry
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| Research Institution | Osaka City University |
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Principal Investigator |
SATO Eisuke Osaka City University, Medical School, Associate Professor, 大学院・医学研究科, 講師 (60211942)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 2005: ¥1,400,000 (Direct Cost: ¥1,400,000)
Fiscal Year 2004: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | Annexin 1 / Inflammation / peptide / Transgenic mice / neutrophils / superoxide / endotoxin / 腹腔 / プロスタクランジン |
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| Research Abstract |
Annexin 1 is a member of annexin superfamily proteins that bind to membrane phospholipids in a calcium-dependent manner. The N-terminal domains of these proteins have unique properties to exhibit their specific functions in various cells. We previously reported that annexin 1 is particularly abundant in neutrophils where it represents up to 3% of the cytosolic proteins. Because the majority of annexin 1 found in inflammatory tissues is associated with neutrophils, this protein might play important roles in the modulation of inflammatory processes. To analyze the physiological roles of annexin 1, we established human annexin1-transgenic mice. The transgenic mice had normal. phenotype and reproduction. Superoxide generation from neutrophils of annexin 1-transgenic mice slightly decreased. The population of neutrophils in blood also decreased. Annexin 1-transgenic mice dramatically blocks lipopolysaccharide (LPS)-stimulated neutrophil migration. Furthermore, we show that neutrophils recruitment induced by casein is suppressed also in annexin 1-transgenic mice. Based on such observations, physiological roles of annexin 1 in vivo will be discussed.
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