The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils
碩士 === 長庚大學 === 天然藥物研究所 === 94 === Cytochalasin B (CB), an actin disrupting agent derived from fungi, has been suggested that it potentiates the effects of chemoattractants such as ROS production, aggregation, and degranulation in neutrophils. However, we do not know whether CB potentiates fMLP-ind...
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ndltd-TW-094CGU005530022015-12-21T04:04:53Z http://ndltd.ncl.edu.tw/handle/13261356346995024727 The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils 探討cytochalasinB加強fMLP誘發人類嗜中性白血球表現的機轉 Wang Mei Ying 王鎂盈 碩士 長庚大學 天然藥物研究所 94 Cytochalasin B (CB), an actin disrupting agent derived from fungi, has been suggested that it potentiates the effects of chemoattractants such as ROS production, aggregation, and degranulation in neutrophils. However, we do not know whether CB potentiates fMLP-induced MAC-1 expression. In present study, we demonstrated that CB potentiated fMLP-induced Mac-1 expression in human neutrophils. This effect can be inhibited by pretreatment of jasplakinolide (a stabilizer of filamentous actin) , colchicine (a degranulation inhibitor), BDM (a endosome recycling inhibitor), SB203580 (a p38 inhibitor), wortmannin (a PI3K inhibitor), genistein (a tyrosine kinase inhibitor), and pertussis toxin (a G-protein coupled receptor inhibitor) but not BAPTA (a calcium chealater), PD98059 (an erk 1/2 inhibitor), staurosporine (a PKC inhibitor), and superoxide dismutase (SOD), suggested multiple signal transduction pathway and granule release involved in this process. CB markedly increased intracellular calcium level and enhanced phosphorylation of tyrosine, erk 1/2, p38, and Akt caused by fMLP. In addition, the deactivated formyl peptide receptor (FPR) can be reactivated by CB and this effect can be inhibited by jasplakinolide and colchicine. Surprisingly, F-actin polymerization induced by fMLP was also potentiated by CB and was inhibited by pretreatment of jasplakinolide, colchicine, BDM, SB203580, wortmannin, genistein, and pertussis toxin. In conclusion, the mechanism of CB potentiation of Mac-1 expression induced by fMLP including regulation of FPR reactivation, potentiation of downstream signaling pathway from reactivated receptor, and granule release. 廖長輝 2006 學位論文 ; thesis 71 zh-TW |
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碩士 === 長庚大學 === 天然藥物研究所 === 94 === Cytochalasin B (CB), an actin disrupting agent derived from fungi, has been suggested that it potentiates the effects of chemoattractants such as ROS production, aggregation, and degranulation in neutrophils. However, we do not know whether CB potentiates fMLP-induced MAC-1 expression. In present study, we demonstrated that CB potentiated fMLP-induced Mac-1 expression in human neutrophils. This effect can be inhibited by pretreatment of jasplakinolide (a stabilizer of filamentous actin) , colchicine (a degranulation inhibitor), BDM (a endosome recycling inhibitor), SB203580 (a p38 inhibitor), wortmannin (a PI3K inhibitor), genistein (a tyrosine kinase inhibitor), and pertussis toxin (a G-protein coupled receptor inhibitor) but not BAPTA (a calcium chealater), PD98059 (an erk 1/2 inhibitor), staurosporine (a PKC inhibitor), and superoxide dismutase (SOD), suggested multiple signal transduction pathway and granule release involved in this process. CB markedly increased intracellular calcium level and enhanced phosphorylation of tyrosine, erk 1/2, p38, and Akt caused by fMLP. In addition, the deactivated formyl peptide receptor (FPR) can be reactivated by CB and this effect can be inhibited by jasplakinolide and colchicine. Surprisingly, F-actin polymerization induced by fMLP was also potentiated by CB and was inhibited by pretreatment of jasplakinolide, colchicine, BDM, SB203580, wortmannin, genistein, and pertussis toxin. In conclusion, the mechanism of CB potentiation of Mac-1 expression induced by fMLP including regulation of FPR reactivation, potentiation of downstream signaling pathway from reactivated receptor, and granule release.
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author2 |
廖長輝 |
author_facet |
廖長輝 Wang Mei Ying 王鎂盈 |
author |
Wang Mei Ying 王鎂盈 |
spellingShingle |
Wang Mei Ying 王鎂盈 The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
author_sort |
Wang Mei Ying |
title |
The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
title_short |
The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
title_full |
The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
title_fullStr |
The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
title_full_unstemmed |
The potential mechamisms of cytochalasin B on fMLP-induced Mac-1 up-regulation in human neutrophils |
title_sort |
potential mechamisms of cytochalasin b on fmlp-induced mac-1 up-regulation in human neutrophils |
publishDate |
2006 |
url |
http://ndltd.ncl.edu.tw/handle/13261356346995024727 |
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