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Gene expression profile of mouse ES cells treated with 1mM valproic acid for 8 hours

ABSTRACT: Histone deacetylase inhibitors (HDACi) cause hyperacetylation of bulk histones and H3K4 hypermethylation in a variety of cell types. They find clinical application as anti-epileptics and chemotherapeutic agents, but the pathways through which they alter cell physiology remain unclear. Surprisingly, changes in gene expression caused by HDACi are often limited in extent and can be positive or negative. Here we have explored the ability of the clinically important HDACi valproic acid (VPA) to alter gene expression in mouse embryonic stem (ES) cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE45610 | GEO | 2013/03/29

SECONDARY ACCESSION(S): PRJNA195397

REPOSITORIES: GEO

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Gene expression profile of mouse ES cells treated with 1mM valproic acid for 8 hours

Project description:Histone deacetylase inhibitors (HDACi) cause hyperacetylation of bulk histones and H3K4 hypermethylation in a variety of cell types. They find clinical application as anti-epileptics and chemotherapeutic agents, but the pathways through which they alter cell physiology remain unclear. Surprisingly, changes in gene expression caused by HDACi are often limited in extent and can be positive or negative. Here we have explored the ability of the clinically important HDACi valproic acid (VPA) to alter gene expression in mouse embryonic stem (ES) cells. CCE/R mouse embryonic stem cells were treated with 1mM valproic acid for 8 hours. Four biological replicates were carried out. Treated cells were labelled with Cy5 and untreated controls with cy3 except in replicate 4 which was a dye-swap.

2013-03-29 | E-GEOD-45610 | biostudies-arrayexpress

Transcriptional response to histone deacetylase inhibitors

Project description:Histone deacetylase inhibitors are a class of drug which rapidly induce hyperacetylation of histone proteins. Here, we aimed to study the association between HDACi-induced histone acetylation and changes in gene expression. To study the early responses to HDACi treatment we treated cells with three different concentrations of two HDACi, sodium valproate (VPA) and suberoylanilide hydroxamic acid over a short timecourse. AH LCL cells were treated with 0.2mM, 1mM or 5mM valproic acid (VPA) or 0.5, 2.5 or 12.5µM suberoylanilide hydroxamic acid (SAHA). GM12878 cells were treated with 1mM VPA. Samples were collected at 0, 30, 60 and 120 minutes. All experiments were carried out in triplicate. One replicate of AH LCL, 0.2mM VPA, 30min and one replicate of AH LCL, 5mM VPA, 30min were eliminated as outliers

2015-08-31 | E-GEOD-65297 | biostudies-arrayexpress

Expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed gene expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2016-04-07 | E-MTAB-3764 | biostudies-arrayexpress

miRNA expression data from human hepatic stellate cell line LX2 treated with suberoylanilide hydroxamic acid (SAHA) or valproic acid (VPA)

Project description:Suberoylanilide hydroxamic acid (SAHA) and valproic acid (VPA ) are both histone deacetylases inhibitor (HDACi), and are able to attenuate the activation of hepatic stelllate cells. To explore the underlying molecular mechanisms, we performed miRNA expression profile analyses of human hepatic stellate cell line LX2 treated with SAHA or VPA for 24 hours. Duplicate experiments were performed: Untreated LX2, SAHA treated LX2 and VPA treated LX2.

2019-07-20 | E-MTAB-6752 | biostudies-arrayexpress

Transcription profiling of human chronic lymphocytic leukemia cells treated with valproic acid

Project description:Epigenetic code modifications by histone deacetylase inhibitors (HDACi) have recently been proposed as potential new therapies for hematological malignancies. Chronic Lymphocytic Leukemia (CLL) remains incurable despite the introduction of new treatments. CLL cells are characterized by an apoptosis defect rather than excessive proliferation, but proliferation centers have been found in organs such as bone marrow and lymph nodes. Here, we investigated gene expression modifications in CLL cells following treatment with valproic acid (VPA), a well-tolerated anti-epileptic drug with HDAC inhibitory activity. Experiment Overall Design: CLL cells obtained from 14 patients were treated in vitro with a concentration of 1mM VPA for 4 hours. VPA effects on gene expression were thereafter studied using Affymetrix technology

2009-09-17 | E-GEOD-14973 | biostudies-arrayexpress

Identification differentially expressed genes upon valproic acid treatment

2011-07-13 | GSE30517 | GEO

A Window of Opportunity Study of Valproic Acid in Breast Cancer Testing a Gene Expression Biomarker

Project description:Purpose: Valproic acid(VPA) has anti-cancer activity attributed to histone deacetylase inhibition(HDACi). We published the Genomically–Derived Sensitivity Signature for VPA(GDSS-VPA), a gene expression biomarker predicting breast cancer sensitivity to VPA in vitro and in vivo. We conducted a window-of-opportunity study examining the tolerability of VPA and the ability of the GDSS-VPA to predict biologic changes in breast tumors from VPA. Methods: Eligible women had untreated breast cancer with breast tumors over 1.5 cm. After a biopsy, women took VPA for 7-12 days, increasing from 30mg/kg/day PO divided BID to a maximum of 50mg/kg/day. After VPA treatment, serum VPA level was measured followed by breast surgery or a biopsy. Tumor proliferation was assessed by Ki-67 immunohistochemistry. Peripheral blood mononuclear cells(PBMCs) histone acetylation was assessed by Western blot. Results: Thirty women were evaluable. The median age was 54(range 31-73). 52% of women tolerated 50mg/kg/day, but 10% missed more than two doses due to adverse events(AEs). Grade 3 AEs included one patient with vomiting and diarrhea and one with fatigue. The end serum VPA level correlated with change in PBMC histone acetylation(rho=0.451, p=0.024). 50% of women with triple-negative breast cancer(TNBC) had a Ki-67 reduction of at least 10%, compared with 17% of other women. GDSS-VPA correlated with a Ki-67 decrease of at least 10%(AUC 0.66). Conclusions: Most women tolerate VPA. VPA treatment caused a decrease in proliferation of breast tumors. The genomic biomarker correlated with decreased proliferation. HDACi is a valid strategy for drug development in TNBC using gene expression biomarkers.

2016-12-17 | GSE83530 | GEO

In Vivo Chemical Screen Nominates Valproic Acid as Pharmacologic Modulator of Hematopoietic Stem and Progenitor Cell Activity

Project description:The identification of small molecules which either increase the number and/or enhance the activity of CD34+ hematopoietic stem and progenitor cells (HSPCs) during ex-vivo expansion has remained challenging. Applying an unbiased in vivo chemical screen in a transgenic (c-myb:EGFP) zebrafish embryo model, histone deacetylase inhibitors (HDACI) (valproic acid, resminostat and entinostat) were shown to significantly amplify the number of phenotypic hematopoietic precursors. The identified HDACIs were confirmed to significantly enhance also the expansion of human HSPCs during ex vivo treatment. Long-term functionality of ex vivo expanded human HSPCs was verified in a xenotransplantation model using NSG mice. However, the HDACI induced proliferation of HSPCs was associated with short-term functional changes. One of the identified hits, valproic acid (VPA), increased the adhesion capacity of CD34+ cells on primary mesenchymal stromal cells and reduced their chemokine-mediated migration capacity in vitro. In line with the reduced migratory potential in vitro, homing as well as early engraftment of VPA treated human CD34+ cells was significantly impaired in the xenotransplantation model. Our data confirms that HDACI treatment leads to a net expansion of HSPCs cells with long-term engraftment potential across different species. However impaired homing and short-term-engraftment has to be kept in mind when designing clinical transplantation protocols. In addition, our gene expression analysis (RNA-Seq) revealed expression of several genes that were altered in CD34+ cells by VPA treatment including cell adhesion molecules and Notch and wnt genes which has been shown to be involved in preservation of stem cell properties.

2017-11-01 | GSE90552 | GEO

Identification differentially expressed genes upon valproic acid treatment

Project description:The goal of this study is to define genes that are differentially expressed in Down syndrome leukemic blasts after treatment with valproic acid (VPA) Here we report the identification gene sets that are downregulated in Down syndrome leukemic cell lines after exposure to valproic acid (VPA) CMK and CMY cells were treated with VPA for 24h and 48h with 1mM or 2mM VPA. Their gene expression profile was compared against the untreated control.

2011-07-12 | E-GEOD-30517 | biostudies-arrayexpress

human placenta-derived cell line (JEG-3): Control vs. valproic acid(VPA)-treated

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.

2012-10-11 | E-GEOD-41441 | biostudies-arrayexpress

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