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Blood, 15 February 2007, Vol. 109, No. 4, pp. 1373-1380.
Prepublished online as a Blood First Edition Paper on October 24, 2006; DOI 10.1182/blood-2006-02-003418.
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CHEMOKINES, CYTOKINES, AND INTERLEUKINS
Histone deacetylase inhibitors suppress IFN -induced up-regulation of promyelocytic leukemia protein
Jana Vlasáková1,
Zora Nováková1,
Lenka Rossmeislová1,
Michal Kahle1,
Pavel Hozák1, and
Zden k Hodn 1
1 Department of Cell Ultrastructure and Molecular Biology, Institute of Experimental Medicine, Academy of Sciences of the Czech Republic, Prague, Czech Republic
Promyelocytic leukemia nuclear bodies (PML NBs), the structural domains of the eukaryotic cell nucleus, play a role in cancer and apoptosis, and their involvement in antiviral mechanisms mediated by interferons (IFNs) is proposed. IFNs dramatically increase the transcription of the PML gene. In this study, we have shown that the response of 2 structural PML NB components, PML and Sp100, to interferon- (IFN) was suppressed in cells simultaneously treated with histone deacetylase (HDAC) inhibitors (trichostatin A, sodium butyrate, MS-275, SAHA, and valproic acid). Trichostatin A (TSA) blocked the increase of PML NB number and suppressed up-regulation of PML mRNA and protein levels in several human cell lines and in normal diploid skin fibroblasts. Moreover, IFN induction of IRF-1 was also inhibited by TSA, although incompletely. Analysis of cellular fractions did not show any defects in cytoplasmic-nuclear transport of STAT2, a component of transcription factor ISGF3 responsible for IFN/ß-dependent gene transcription. Moreover, chromatin immunoprecipitation showed that after IFN stimulation STAT2 binds to ISRE element of PML promoter even in the presence of TSA and thus excluded STAT2-dependent mechanism of TSA effect. These results indicate that the action of histone deacetylases is necessary for the full transcriptional activation of IFN-stimulated genes.
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