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N-formyl-Met-Leu-Phe-induced oxidative burst in DMSO-differentiated HL-60 cells requires active Hsp90, but not intact microtubules
J. Vrba, M. Modrianský
Language English Country Czech Republic
Document type Journal Article, Research Support, Non-U.S. Gov't
NLK
Directory of Open Access Journals
from 2001
Free Medical Journals
from 1998
ROAD: Directory of Open Access Scholarly Resources
from 2001
PubMed
15744362
DOI
10.5507/bp.2004.025
Knihovny.cz E-resources
- MeSH
- Cell Differentiation MeSH
- Dimethyl Sulfoxide pharmacology MeSH
- HL-60 Cells MeSH
- Colchicine pharmacology MeSH
- Humans MeSH
- Microtubules drug effects physiology MeSH
- N-Formylmethionine Leucyl-Phenylalanine pharmacology MeSH
- Neutrophils metabolism MeSH
- Nocodazole pharmacology MeSH
- Paclitaxel pharmacology MeSH
- HSP90 Heat-Shock Proteins metabolism MeSH
- Respiratory Burst drug effects MeSH
- Dose-Response Relationship, Drug MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
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.
References provided by Crossref.org
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