Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA275706 | ENA |
REPOSITORIES: ENA
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Project description:Histone deacetylase (HDAC) inibitors suppress cell proliferation of prostate cancer, but the detailed mechanisms are unknown. Moreover, HDAC includes 18 family members, namely HDAC1-11 and SIRT1-7, and differences of effects on prostate cancer proliferation among these enzymes are also unknown. Thus, we clarified differences of gene expression between prostate cancer cell line (LNCaP) treated with pan-HDAC inhibitors (TSA and OBP-801) or selective HDAC inhibitor (NCC-149, HDAC8-specific inhibitor)using cDNA microarray. LNCaP treated with TSA (1μM), NCC149 (2μM), OBP-801 (200nM) or DMSO for 24hrs, RNA was extracted from cells, and cDNA array was performed.
2015-11-04 | E-GEOD-74418 | biostudies-arrayexpress
Project description:Genome wide expression changes following treatment with the HDACs (Histone Deacetylase Inhibitor) CG-1521 (7.5uM) or TSA (Trichostatin A) were investigated to determine regulatory targets and patterns of the HDAC Inhibitors. LNCaP Prostate Cancer cells were treated for a period of 24h with either CG-1521 (7.5uM) or TSA (5uM) following a 24h seeding period. At the selected time point, total RNA was harvested from the cells for hybridization and analysis by Nimblgen Systems Inc using the homo sapiens gene expression array.
2007-09-15 | E-GEOD-8645 | biostudies-arrayexpress
Project description:Genome wide expression changes following treatment with the HDACs (Histone Deacetylase Inhibitor) CG-1521 (7.5uM) or TSA (Trichostatin A) were investigated to determine regulatory targets and patterns of the HDAC Inhibitors. Keywords: Expression response to treatment, data was used for a comparison of gene expression and regulation between CG-1521 and TSA in LNCaP Cells
2007-09-15 | GSE8645 | GEO
Project description:Trichostatin A (TSA) is one of the most potent reversible histone deacetylase (HDAC) inhibitors. In male mice, subcutaneous application of TSA is followed by infertility due to apoptosis of pachytene spermatocytes. To get more insight into the mechanisms underlying this phenomenon, we performed a genome-wide expression analysis of murine testes after TSA treatment. The whole genome transcriptome analysis revealed 507 significantly regulated genes. Validation by real-time quantitative PCR confirmed the expression of 7 from 9 genes tested (78%). Keywords: time course
2007-08-02 | GSE5448 | GEO
Project description:Cardiac hypertrophy is characterized by an increase in heart size and profound gene expression changes. Pharmacological histone deacetylase (HDAC) inhibitors attenuate pathological cardiac remodeling and hypertrophic gene expression. Published literature has linked enzymes that mediates histone acetylation to pathogenesis, however, the role of histone acetylation to define hypertrophic gene regulatory events are not well understood. We used chromatin immunoprecipitation (ChIP) coupled with massive parallel sequencing (seq) to comprehensively examine genome-wide histone acetylation changes in a pre-clinical model of pathological cardiac hypertrophy by transverse aortic constricted (TAC). We examined the gene targets conferred by the prototypical HDAC inhibitor Trichostatin A (TSA). TSA induces genome-wide histone acetylation and deacetylation in the heart. Alterations to histone acetylation were found on genes involved in cardiac morphology such as cardiac contraction, collagen deposition, inflammation and extracellular matrix. Gene set enrichment analysis identified NF-kappa B (NFKB), as a transcription factor positively correlated with TAC and negatively correlated with TSA by ChIP-seq. Histone acetylation on the promoters of NKFB target genes was increased, consistent with gene activation. In contrast, the promoters of these genes were deacetylated by TSA in hypertrophic animals and reduced expression of NFKB target genes. Our results suggest a potential mechanism for TSA mediated cardioprotection conferred by histone deacetylation of target genes implicating the importance of inflammation. ChIP-seq profiles for histone acetylation in left ventricles of mice that develop cardiac hypertrophy and treated with HDAC inhibitors were generated by deep sequencing, using Illumina GAIIx.
2015-04-25 | E-GEOD-63590 | biostudies-arrayexpress
Project description:Histone deacetylase inhibitors (HDACis) have been shown to potentiate hippocampal-dependent memory and synaptic plasticity and to ameliorate cognitive deficits and degeneration in animal models for different neuropsychiatric conditions. However, the impact of these drugs on hippocampal histone acetylation and gene expression profiles at the genomic level, and the molecular mechanisms that underlie their specificity and beneficial effects in neural tissue, remains obscure. Here, we mapped four relevant histone marks (H3K4me3, AcH3K9,14, AcH4K12 and pan-AcH2B) in hippocampal chromatin and investigated at the whole-genome level the impact of HDAC inhibition on acetylation profiles and basal and activity-driven gene expression. HDAC inhibition caused a dramatic histone hyperacetylation that was largely restricted to active loci pre-marked with H3K4me3 and AcH3K9,14. In addition, the comparison of Chromatin immunoprecipitation sequencing and gene expression profiles indicated that Trichostatin A-induced histone hyperacetylation, like histone hypoacetylation induced by histone acetyltransferase deficiency, had a modest impact on hippocampal gene expression and did not affect the transient transcriptional response to novelty exposure. However, HDAC inhibition caused the rapid induction of a homeostatic gene program related to chromatin deacetylation. These results illuminate both the relationship between hippocampal gene expression and histone acetylation and the mechanism of action of these important neuropsychiatric drugs. We performed transcriptional profiling of hippocampal samples from willd-type and cbp+/- mice (C57/DBA F1 hybrid females). Treatments consisted in intraperioneal treatment with HDACi TSA (2.4 mg/kg) o vehicle (DMSO/Saline). Samples were obtained 75 min after TSA administration. Novelty consisted of placing an individual animal in a white plexiglas square box containing plastic tubing and small toys for 1h. For TSA and Novelty condition animals were injected with TSA and 15 min later were allowed to exploration in the Novelty paradigm. We obtained quintuplicate (standar housing) and triplicate (novelty; TSA; and novelty + TSA) samples containing total RNA from the hippocampi of 3-4 three-month old females of either genotype (cbp+/- and wild-type mice) (in total >100 mice were used in the experiment).
2013-07-09 | E-GEOD-43051 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE3783: Trichostatin A (TSA) inhibition of histone deacetylase in Arabiodopsis thaliana; GSE3784: Seed germination in presence and absence of histone deaceatylase inhibitor, Trichostain A (TSA). Histone acetylation is involved in the regulation of gene expression in plants and eukaryotes. Histone deacetylases (HDACs) are enzymes that catalyze the removal of acetyl groups from histones, which is associated with the repression of gene expression. To study the role of histone acetylation in the regulation of gene expression during seed germination, trichostatin A (TSA), a specific inhibitor of histone deacetylase, was used to treat imbibing Arabidopsis thaliana seeds. GeneChip arrays were used to show that TSA induces up-regulation of 45 genes and down-regulation of 27 genes during seed germination. Eight TSA-up-regulated genes were selected for further analysis - RAB18, RD29B, ATEM1, HSP70 and four late embryogenesis abundant protein genes (LEA). A gene expression time course shows that these eight genes are expressed at high levels in the dry seed and repressed upon seed imbibition at an exponential rate. In the presence of TSA, the onset of repression of the eight genes is not affected but the final level of repressed expression is elevated. Chromatin immunoprecipitation and HDAC assays show that there is a transient histone deacetylation event during seed germination at one day after imbibition, which serves as a key developmental signal that affects the repression of the eight genes. Experiment Overall Design: Refer to individual Series
2008-06-12 | E-GEOD-3799 | biostudies-arrayexpress
Project description:Histone acetylation is involved in the regulation of gene expression in plants and eukaryotes. Histone deacetylases (HDACs) are enzymes that catalyze the removal of acetyl groups from histones, which is associated with the repression of gene expression. To study the role of histone acetylation in the regulation of gene expression during seed germination, trichostatin A (TSA), a specific inhibitor of histone deacetylase, was used to treat imbibing Arabidopsis thaliana seeds. GeneChip arrays were used to show that TSA induces up-regulation of 45 genes and down-regulation of 27 genes during seed germination. Eight TSA-up-regulated genes were selected for further analysis - RAB18, RD29B, ATEM1, HSP70 and four late embryogenesis abundant protein genes (LEA). A gene expression time course shows that these eight genes are expressed at high levels in the dry seed and repressed upon seed imbibition at an exponential rate. In the presence of TSA, the onset of repression of the eight genes is not affected but the final level of repressed expression is elevated. Chromatin immunoprecipitation and HDAC assays show that there is a transient histone deacetylation event during seed germination at one day after imbibition, which serves as a key developmental signal that affects the repression of the eight genes. Keywords: histone deacetylase inbibition, developmental effects
2005-12-10 | GSE3784 | GEO
Project description:Histone acetylation is involved in the regulation of gene expression in plants and eukaryotes. Histone deacetylases (HDACs) are enzymes that catalyze the removal of acetyl groups from histones, which is associated with the repression of gene expression. To study the role of histone acetylation in the regulation of gene expression during seed germination, trichostatin A (TSA), a specific inhibitor of histone deacetylase, was used to treat imbibing Arabidopsis thaliana seeds. GeneChip arrays were used to show that TSA induces up-regulation of 45 genes and down-regulation of 27 genes during seed germination. Eight TSA-up-regulated genes were selected for further analysis - RAB18, RD29B, ATEM1, HSP70 and four late embryogenesis abundant protein genes (LEA). A gene expression time course shows that these eight genes are expressed at high levels in the dry seed and repressed upon seed imbibition at an exponential rate. In the presence of TSA, the onset of repression of the eight genes is not affected but the final level of repressed expression is elevated. Chromatin immunoprecipitation and HDAC assays show that there is a transient histone deacetylation event during seed germination at one day after imbibition, which serves as a key developmental signal that affects the repression of the eight genes. Keywords: histone deacetylase inhibitor, developmental effects
2005-12-10 | GSE3783 | GEO
Project description:Histone acetylation alters the chromatin state and thus gene expression and cellular activities. In spite of various applications of Histone Deacetylase inhibitors (DACIs) their mechanism or selectivity is not fully understood. We studied the mechanism by which the DACI Trichostatin A upregulates the MHC class II DRA gene in RJ225 cells lacking CIITA. We show that TSA increases HDAC1 and 2 protein mobility and reduces their recruitment to the DRA promoter. Coordinated chromatin changes are manifested by increasing H3 K4 methylation and decreasing K9 methylation, leading to elevated RNA PolII recruitment and the onset of transcription. Gene expression profiling showed that diverse TSA responsive gene groups, including the highly upregulated the MHC class II family and the adjacent histone cluster are located in chromosome 6p21-22. A complex pattern of gene reprogramming by TSA involves immune recognition, antiviral, apoptotic and inflammatory pathways and extends the rationale for using DACIs to modulate the immune response.
2006-08-07 | E-MEXP-403 | biostudies-arrayexpress