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Effect of valproic acid on hematopoiesis: A functional profiling and cell phenotyping approach

ABSTRACT: Analysis of the effects of valproic acid (VPA) on chronic myelogenous leukemia K562 cells. This study attempts to elucidate the effects of VPA on cell homeostasis and hematopoietic differentiation pathways in this cell line.

ORGANISM(S): Homo sapiens

PROVIDER: GSE19939 | GEO | 2010/12/01

SECONDARY ACCESSION(S): PRJNA122631

REPOSITORIES: GEO

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Effect of valproic acid on hematopoiesis: A functional profiling and cell phenotyping approach

Project description:Analysis of the effects of valproic acid (VPA) on chronic myelogenous leukemia K562 cells. This study attempts to elucidate the effects of VPA on cell homeostasis and hematopoietic differentiation pathways in this cell line. We used ten experimental conditions comparing valproic acid-treated and untreated cells at time points 2, 6, 10, 48 and 72 hrs respectively. Experiments were performed in three biological replicates including a dye swap (represented by replicate 3, for each timepoint).

2010-12-01 | E-GEOD-19939 | biostudies-arrayexpress

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

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

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Effect of Valproic Acid on Endothelial Cells

Project description:Valproic acid (VPA) is a short-chain fatty acid used in the treatment of epilepsy and also considered to be an epigenetic modifier by functioning as a histone deacetylase (HDAC)-inhibitor. The aim of this study was to search for gene altered by VPA in human endothelial cells.

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The effect of valproic acid in BMDMs

Project description:Currently, the clinical role and influence of valproic acid (VPA) on bone homeostasis remains controversial. In the current study, we confirmed that VPA treatment was linked to a decrease in bone mass and bone mineral density (BMD), an effect that is hypothesized to be caused by a VPA-induced elevation in osteoclast formation and activity. RNA-sequencing revealed a prominent increase of miR-6359 expression in VPA-treated osteoclast precursors which has been demonstrated to be responsible for osteoclast differentiation and bone-resorptive activity. VPA-induced miR-6359 upregulation in osteoclast precursors enhanced ROS production by silencing the SIRT3 protein level, followed by activating the MAPK signaling pathways, which promoted osteoclast formation and activity, thereby accelerating bone loss.

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Effects of prenatal valproic acid exposure on hippocampal gene expression after birth

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Expression data from untreated and valproic acid (VPA) treated CD34+ Hematopoietic Stem Cells (HSCs)

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.

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