Effects of VPA in P19KO embryos
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA733173 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR14668221.fastq.gz | Fastqsanger.gz | |||
| SRR14668222.fastq.gz | Fastqsanger.gz | |||
| SRR14668223.fastq.gz | Fastqsanger.gz | |||
| SRR14668224.fastq.gz | Fastqsanger.gz | |||
| SRR14668225.fastq.gz | Fastqsanger.gz |
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Project description:To identify genes that are induced by Valproic acid in E8.5 mouse embryos, and how these genes are altered in p19-deficient embryos
2022-05-12 | GSE175680 | GEO
Project description:Background: Histone deacetylase (HDAC) is strongly associated with epigenetic regulation and carcinogenesis, and its inhibitors induce the differentiation or apoptosis of cancer cells. Valproic acid (VPA) is one of the clinically available HDAC inhibitors. We investigated the anticancer effects of VPA in combination with gemcitabine (GEM) in cholangiocarcinoma cell line, and explored the mechanisms of the anticancer effects using microarray analysis. Methods: A human cholangiocarcinoma cell line (HuCCT1) was used. The anticancer effects of VPA, or gemcitabine (GEM), and the effects of VPA combined with GEM, were studied by cell proliferation assay. The microarray analysis was performed, the genes were picked up using Gene Spring GX11.5, Ingenuity Pathways Analysis (IPA) was performed, and then the gene-expression was determined by RT-PCR. Results: GEM (5nM) and VPA (0.5mM) reduced by 23%, which significantly augmented the anticancer effect of GEM alone or VPA alone (P<0.01). Using the microarray analysis, forty-three genes were identified with the comparison between GEM group and GEM plus VPA combination group. The interactions were shown between genes of the “Cellular Development” relevant to the differentiation of cancer cell using IPA.
2011-02-09 | GSE27036 | GEO
Project description:Histone deacetylase (HDAC) inhibitors are widely utilized in hematopoietic malignance therapy; nevertheless, little is currently known concerning their effects on normal myelopoiesis. In order to investigate a putative interference of HDAC inhibitors in myeloid commitment of hematopoietic stem/progenitor cells (HSPCs) we treated CD34+ cells with valproic acid (VPA). Moreover, we investigate changes in gene expression induced by VPA treatment on HSPCs, by means of microarray analysis in VPA treated and untreated (CTR) CD34+ cells. VPA treatment induced H4 histone acetylation in CD34+ cells and blocked them in G0-G1 phase of cell cycle. CD34 expression is maintained for a longer time in VPA treated cells, while the physiological decrease of CD34 antigen occurred in CTR cells. Moreover, VPA favored erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage lineages, as demonstrated by immunophenotyping, morphological and clonogenic analysis. Finally, we demonstrated that VPA up-regulated master gene regulators of erythrocyte and megakaryocyte differentiation (GFI1B and MLLT3) through histone iper-acetylation of their promoters. These results indicate that VPA treatment enhances erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage one. Microarray data provide for the first time a detailed molecular support for the biological effects promoted by VPA treatment in HSPCs.
2013-04-11 | GSE31283 | GEO
Project description:Background: Histone deacetylase (HDAC) is strongly associated with epigenetic regulation and carcinogenesis, and its inhibitors induce the differentiation or apoptosis of cancer cells. Valproic acid (VPA) is one of the clinically available HDAC inhibitors. We investigated the anticancer effects of VPA in combination with gemcitabine (GEM) in cholangiocarcinoma cell line, and explored the mechanisms of the anticancer effects using microarray analysis. Methods: A human cholangiocarcinoma cell line (HuCCT1) was used. The anticancer effects of VPA, or gemcitabine (GEM), and the effects of VPA combined with GEM, were studied by cell proliferation assay. The microarray analysis was performed, the genes were picked up using Gene Spring GX11.5, Ingenuity Pathways Analysis (IPA) was performed, and then the gene-expression was determined by RT-PCR. Results: GEM (5nM) and VPA (0.5mM) reduced by 23%, which significantly augmented the anticancer effect of GEM alone or VPA alone (P<0.01). Using the microarray analysis, forty-three genes were identified with the comparison between GEM group and GEM plus VPA combination group. The interactions were shown between genes of the “Cellular Development” relevant to the differentiation of cancer cell using IPA. Total RNA was isolated from both the stimulated and unstimulated cells (HuCCT-1) using RNeasy Mini kit (Qiagen, Valencia, CA). Relative purity was examined using an Agilent 2100 Bioanalyzer (Agilent Technologies, Santa Clara, CA, USA). RNA expression was analyzed using GeneChip○R Human Gene 1.0 ST Array (Affymetrix, Santa Clara, CA, USA), containing 28,869 oligonucleotide probes for known and unknown genes. First standard cDNA was synthesized from 300 ng of total RNA by using GeneChip○R Whole Transcript (WT) cDNA Synthesis and Amplification Kit (Affymetrix) according to the manufacturer’s instructions. 10 μg of cRNA were input into the second-cycle cDNA reaction. cDNA was fragmented and end-labeled with the GeneChip○R WT Terminal Labeling Kit (Affymetrix). Approximately 5.5μg of fragmented and labeled DNA target was hybridized to the Affymetrix GeneChip○R Human Gene 1.0 ST Array at 45°C for 17h on a GeneChip○R Hybridization Oven 640 (Affymetrix) according to the manufacturer’s recommendation. Hybridized arrays were washed and stained on a GeneChip○R Fluidics Station 450 and scanned on a GeneChip○R Scanner 3000 7G (Affymetrix), and then generated CEL files for each array. The microarray data was normalized by GeneSpring GX 11.5 software (Agilent). The cut-off value was set at 0.5 to 2.0 for the ratio (more than 2.0: up-regulation, 0.5-2.0: no change, less than 0.5: down-regulation). Gene Ontology (GO) was analyzed using GeneSpring GX 11.5 software (Agilent), and p-value < 0.05 was used for significance. Then we used Ingenuity Pathway Analysis (IPA) 8.7 (http://www.ingenuity.com) to determine the functional pathways associated with the set of differentially expressed genes between genotypes. IPA utilizes the knowledge in the literature about biological interactions among genes and proteins.
2011-02-09 | E-GEOD-27036 | biostudies-arrayexpress
Project description:Genome-wide maps of the H3K9 acetylation state in embryonic stem cells (ESCs) before and after treatment with low levels of the histone deacetylase (HDAC) inhibitor valproic acid (VPA). ChIP-seq for 3 samples: untreated E14 cells, cells treated with VPA for 4 hrs and cells treated with VPA for 16 hrs. Unprecipitated DNA was used as the input control (Input).
2011-09-17 | E-GEOD-24211 | biostudies-arrayexpress
Project description:Valproic acid (VPA) is a potent inducer of neural tube defects (NTDs), but its mechanism of teratogenicity is not known. To study the transcriptional response of VPA during the susceptible period, i.e. when VPA is likely to exert most of its teratogenic effect, RNA was extracted from 8.25-dpc embryos (6 h post treatment) from control and VPA-treated dams, and subjected to microarray analysis (four arrays). To be more useful for risk assessment, in vitro models, using cells, may bridge biomarkers discovered by gene expression profiling in an animal in vivo model. Since pluripotent embryocarcinoma (EC) cell lines may be relevant models for early embryonic cells, P19 mouse EC cells were treated with or without 1 mM sodium valproate for 24 h and alos subjected to microarray analysis (four arrays).
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Project description:Histone deacetylase (HDAC) inhibitors are widely utilized in hematopoietic malignance therapy; nevertheless, little is currently known concerning their effects on normal myelopoiesis. In order to investigate a putative interference of HDAC inhibitors in myeloid commitment of hematopoietic stem/progenitor cells (HSPCs) we treated CD34+ cells with valproic acid (VPA). Moreover, we investigate changes in gene expression induced by VPA treatment on HSPCs, by means of microarray analysis in VPA treated and untreated (CTR) CD34+ cells. VPA treatment induced H4 histone acetylation in CD34+ cells and blocked them in G0-G1 phase of cell cycle. CD34 expression is maintained for a longer time in VPA treated cells, while the physiological decrease of CD34 antigen occurred in CTR cells. Moreover, VPA favored erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage lineages, as demonstrated by immunophenotyping, morphological and clonogenic analysis. Finally, we demonstrated that VPA up-regulated master gene regulators of erythrocyte and megakaryocyte differentiation (GFI1B and MLLT3) through histone iper-acetylation of their promoters. These results indicate that VPA treatment enhances erythrocyte and megakaryocyte differentiation at the expense of granulocyte and mono-macrophage one. Microarray data provide for the first time a detailed molecular support for the biological effects promoted by VPA treatment in HSPCs. Human CD34+ cells were purified from umbilical Cord Blood (CB) samples. After an initial 24 hours of incubation, CD34+ cells were exposed to VPA. Total cellular RNA was extracted from untreated (CTR) and VPA treated CD34+ HSCs after 48 hours of treatment.
2013-04-11 | E-GEOD-31283 | biostudies-arrayexpress
Project description:Transcriptional profiling of human placenta-derived JEG-3 cell line comparing vehicle control with 7.38 mM of valproic acid(VPA)-treated JEG-3 cells for 48 hr. 7.38 mM valproic acid(VPA) induced the 30% inhibiotion of JEG-3 cell proliferation, G1 phase cell cycle arrest and the reduction of cell size. The Goal was to analyze the mechanism of valproic acid-induced adverse effects in placental cells. Two-condition experiment, JEG-3 cells vs. valproic acid(VPA)-treated JEG-3 cells. Biological replicates: 3 control replicates, 3 VPA-treated replicates.
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