N-甲酰甲硫氨酰-亮氨酰-苯丙氨酸诱导二甲基亚砜分化的HL-60细胞产生氧化爆发需要活性热休克蛋白90，但不需要完整的微管。

N-formyl-Met-Leu-Phe-induced oxidative burst in DMSO-differentiated HL-60 cells requires active Hsp90, but not intact microtubules.

作者信息

Vrba Jirí, Modrianský Martin

机构信息

Institute of Medical Chemistry and Biochemistry, Faculty of Medicine, Palacký University, Hnevotínská 3, 775 15 Olomouc, Czech Republic.

出版信息

Biomed Pap Med Fac Univ Palacky Olomouc Czech Repub. 2004 Dec;148(2):141-4.

PMID:15744362

Abstract

In this study we examined whether microtubules and heat shock protein 90 (Hsp90) are involved in phorbol myristate acetate (PMA) and N-formyl-Met-Leu-Phe (fMLP)-induced oxidative burst in DMSO-differentiated HL-60 cells. Our results showed that microtubule interfering agents, paclitaxel (1-5 microM), colchicine (1-100 microM), nocodazole (1-20 microM), and vincristine (1-50 microM), did not affect either PMA or fMLP-induced oxidative burst. In contrast, radicicol, an inhibitor of Hsp90, inhibited fMLP-induced oxidative burst in time and concentration-dependent manner where IC50 value for 30 min pre-incubation was 16.5 +/- 3.5 microM radicicol. We conclude that both PMA and fMLP-induced oxidative burst in DMSO-differentiated HL-60 cells is microtubule-independent while the latter requires Hsp90 activity.

摘要

在本研究中，我们检测了微管和热休克蛋白90（Hsp90）是否参与佛波酯（PMA）和N-甲酰甲硫氨酰亮氨酰苯丙氨酸（fMLP）诱导的二甲基亚砜（DMSO）分化的HL-60细胞中的氧化爆发。我们的结果显示，微管干扰剂紫杉醇（1 - 5 microM）、秋水仙碱（1 - 100 microM）、诺考达唑（1 - 20 microM）和长春新碱（1 - 50 microM），均不影响PMA或fMLP诱导的氧化爆发。相反，Hsp90抑制剂雷迪西可抑制fMLP诱导的氧化爆发，呈时间和浓度依赖性，30分钟预孵育的IC50值为16.5±3.5 microM雷迪西可。我们得出结论，DMSO分化的HL-60细胞中，PMA和fMLP诱导的氧化爆发均不依赖微管，而后者需要Hsp90活性。