CD34+ HSPC CITE-seq for day 0 and Day 1 and Day 4 under VPA
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ABSTRACT:
PROVIDER: PRJNA903209 | ENA |
REPOSITORIES: ENA
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Project description:The regenerative potential of human hematopoietic stem cells (HSCs) is well established by to their ability of life-long blood cell production and cure of a wide range of hematological diseases upon transplantation. This regenerative potential depends on HSC self-renewal and the coordinated adaptation to metabolic stress conditions. This is especially critical during ex vivo culture/manipulation of HSCs that is frequently accompanied with loss of self-renewal potential resulting in stem cell exhaustion. We have previously reported that CD34+ human hematopoietic stem and progenitor cells (HSPC) can be efficiently reprogrammed and expanded to phenotypic HSCs with long-term repopulation capacity in the presence of cytokines and valproic acid (VPA). Here, we present evidence that the SIRT1-SIRT3 axis maintains the mitochondrial activity below a critical threshold by coordinating and retaining a transcriptional and metabolic landscape of human HSCs with long-term self-renewal properties during ex vivo HSC reprogramming.
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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.
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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.
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Project description:The goal of this study is to identify m6A targets in human CD34+ HSPCs with or without STM2457 treatment using DARTseq. Purified human CD34+ HSPC cells were transduced with APOBEC-YTH or empty vector control (MIG). 24hr post infection, CD34+ cells were treated with STM2457 at a concentration of 20µM for 2 days. GFP+ cells were sorted the next day. 3 replicates were performed.
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Project description:Transciptome analysis of CD34+ enriched human HSPC lentivirally transduced with cohesin WT or mutant
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Project description:We demonstrated to examine the effect of AhR antagonists on the specific lineage-biased differentiation of HSPC. To confirm this, CD34+ cells isolated from cord blood were cultured with two antagonists (CH223191 and StemRegenin 1) for 14 days to monitor their phenotype, and chromatin immunoprecipitation DNA was extracted from cultured cells on the 14th day of culture. We sought to explain the relationship between the action of AhR-antagonist complex and the megakaryocyte lineage-biased differentiation of HSPC with these ChIP-seq results.
2022-06-01 | GSE184778 | 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.
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