Mechanism of transendothelial migration of neutrophils
Mechanism of transendothelial migration of neutrophils
批准号:
13671061
负责人:
SASADA Masataka
金额:
$1.98万
依托单位:
依托单位国家:
日本
项目类别:
Grant-in-Aid for Scientific Research (C)
财政年份:
2001
资助国家:
日本
项目状态:
已结题
起止时间:
2001 至 2002
中文摘要
中性粒细胞在骨髓中产生并释放到血液中。然后,它们穿过内皮细胞进入组织。由于中性粒细胞主要在组织中起宿主防御作用,因此跨内皮迁移(TEM)在组织中中性粒细胞的数量受到TEM的调节方面具有重要意义。一氧化氮(NO)已被报道由内皮细胞产生并影响中性粒细胞与内皮细胞的粘附,尽管有一些相互矛盾的报道。我们的研究目的是阐明NO在中性粒细胞TEM中的作用。以下是本研究项目的发现和结果。NO抑制中性粒细胞TEM。补充外源性NO抑制中性粒细胞TEM。NO合成酶抑制剂和NO猝灭剂使中性粒细胞TEM升高。一氧化氮由内皮细胞产生。NO猝灭剂使中性粒细胞TEM升高。NO合成酶抑制剂使中性粒细胞TEM升高。内皮细胞中检测到NO。NO作用于中性粒细胞。中性粒细胞与内皮细胞共培养后,在中性粒细胞中检测到NO。NO激活鸟苷酸环化酶,调节中性粒细胞的TEM。
英文摘要
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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Takano K, Sasada M, et al.: "Rapid and prominent up-regulation of high-affinity receptor far Immunoglobulin G(Fc γ RI) by cross-linking of β2 integrins on polymorphonuclear leukocytes"Int J Hematol. 72(1). 48-54 (2000)
Takano K、Sasada M 等人:“通过多形核白细胞上 β2 整联蛋白的交联,快速、显着地上调高亲和力受体远免疫球蛋白 G (Fc γ RI)”Int J Hematol 72(1)。 48-54 (2000)
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Yamashita K, Sasada M, et al.: "6-formylpterin intracellularly generates hydrogen peroxide and restores the impaired bactericidal activity of human neutrophils"Biochem Biophys Res Commun. 289(1). 85-90 (2001)
Yamashita K、Sasada M 等人:“6-甲酰蝶呤在细胞内产生过氧化氢并恢复人类中性粒细胞受损的杀菌活性”Biochem Biophys Res Commun。
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Kobayashi S, Sasada M, et al.: "Calpain-mediated XIAP degradation in neutrophil apoptosis and its impairment in chronic neutrophilic leukemia"J Biol Chem. 277(37). 33968-33977 (2002)
Kobayashi S、Sasada M 等人:“钙蛋白酶介导的中性粒细胞凋亡中的 XIAP 降解及其对慢性中性粒细胞白血病的损害”J Biol Chem。
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Takano K, Sasada M, et al.: "Rapid and prominent up-regulation of high-affinity receptor for Immunoglobulin G(Fc γ RI) by cross-linking of β 2 integrins on polymorphonuclear leukocytes"Int J Hematol. 72(1). 48-54 (2000)
Takano K、Sasada M 等人:“通过多形核白细胞上 β 2 整联蛋白的交联,快速、显着地上调免疫球蛋白 G (Fc γ RI) 的高亲和力受体”Int J Hematol 72(1)。 .48-54 (2000)
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Arai T, Sasada M, et al.: "6-Formylpterin, a xanthine oxidase inhibitor, intracellularly generates reactive oxygen species involved in apoptosis and cell proliferation"Free Rad Biol Med. 30(3). 248-259 (2001)
Arai T、Sasada M 等人:“6-甲酰蝶呤,一种黄嘌呤氧化酶抑制剂,在细胞内产生参与细胞凋亡和细胞增殖的活性氧”Free Rad Biol Med。
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共 10 条
Transmigration of neutrophils through epithelium
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批准号:15591003
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项目类别:Grant-in-Aid for Scientific Research (C)
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资助金额:$2.24万
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财政年份:2003
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负责人:SASADA Masataka
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依托单位:
海外基金