In vitro DC models
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Kristina Lundberg
PROVIDER: E-MEXP-3787 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To investigate the effects of EDAG knockdown on gene exrpession profile in human cord blood CD34+ cells with EPO treatment with microarray assay. Freshly isolated human cord blood CD34+ cells were pre-activated for 24 hours and then infected with EDAG RNAi lentivirus or control lentivirus for 3 times within 24 hours. Then the cells were cultured in the presence of EPO to induce erythroid differentiation. Four days later, the cells were harvested for microarray test. The microarray showed that 3149 differentially expressed genes in siEDAG group compared to control group.The altered genes were associated with gene exrpression, cell cycle and hematopoietic differentiation. These data show that EDAG knckdown led to down-regulation of erythroid genes which are activated by GATA1. Human CD34+ cells infected with EDAG RNAi or control lentivirus were treated with EPO (5U/ml) for 4 days and gene expression were measured using Agilent human whole Genome 8*60K array. Two replicates.
2013-11-06 | E-GEOD-46720 | biostudies-arrayexpress
Project description:Macrophage activation is associated with profound transcriptional reprogramming. Although much progress has been made in the understanding of macrophage activation, polarization and function, the transcriptional programs regulating these processes remain poorly characterized. We stimulated human macrophages with diverse activation signals, acquiring a dataset of 299 macrophage transcriptomes. Analysis of this dataset revealed a spectrum of macrophage activation states extending the current M1 versus M2-polarization model. Network analyses identified central transcriptional regulators associated with all macrophage activation complemented by regulators related to stimulus-specific programs. Applying these transcriptional programs to human alveolar macrophages from smokers and patients with chronic obstructive pulmonary disease (COPD) revealed an unexpected loss of inflammatory signatures in COPD patients. Finally, by integrating murine data from the ImmGen project we propose a refined, activation-independent core signature for human and murine macrophages. This resource serves as a framework for future research into regulation of macrophage activation in health and disease. Since transcriptional programs are further modulated on several levels including miRNAs we assessed the global spectrum of miRNA expression by miRNA-Seq in macrophages stimulated with IFNM-NM-3, IL4 or with the combination of TNFM-NM-1, PGE2 and P3C
2014-02-13 | E-GEOD-51307 | biostudies-arrayexpress
Project description:Macrophage activation is associated with profound transcriptional reprogramming. Although much progress has been made in the understanding of macrophage activation, polarization and function, the transcriptional programs regulating these processes remain poorly characterized. We stimulated human macrophages with diverse activation signals, acquiring a dataset of 299 macrophage transcriptomes. Analysis of this dataset revealed a spectrum of macrophage activation states extending the current M1 versus M2-polarization model. Network analyses identified central transcriptional regulators associated with all macrophage activation complemented by regulators related to stimulus-specific programs. Applying these transcriptional programs to human alveolar macrophages from smokers and patients with chronic obstructive pulmonary disease (COPD) revealed an unexpected loss of inflammatory signatures in COPD patients. Finally, by integrating murine data from the ImmGen project we propose a refined, activation-independent core signature for human and murine macrophages. This resource serves as a framework for future research into regulation of macrophage activation in health and disease. To better understand active gene regulation in human macrophages during activation and differentiation in vitro with different stimuli ChIP-sequencing experiments were performed. Enrichment patterns of the permissive histone modification mark trimetylation of histone protein 3 (H3K4me3) and macrophage lineage-specific transcription factor PU.1 were analyzed.
2014-02-13 | E-GEOD-47188 | biostudies-arrayexpress
Project description:In order to investigate the mechanism whereby TEL-PDGF-beta (ETV6-PDGFRB) interferes with human hematopoietic progenitors proliferation and differentiation, we analyzed the gene expression response downstream this oncogene. CD34+ cells infected with lentivirus coding for TEL-PDGFRb were cultured for 7 days in the absence of cytokines. Using Affymetrix microarrays, we compared gene expression in these cells and in cells treated for 4 h with low dose imatinib (Glivec), a potent PDGFR inhibitor, to switch off TEL-PDGFRb signaling. This experiment was performed in three biological replicates. In each replicate gene expression profiling from CD34+ HSCs expressing TEL-PDGFRb untreated with Glivec was compared to the corresoniding treated condition. Total RNA were extracted from transduced CD34+ cells using Trizol reagent (Invitrogen) and the RNeasy kit (QIAGEN).
2012-04-09 | E-GEOD-28698 | biostudies-arrayexpress
Project description:Histone modifcations at the p15INK4b gene were compared in sample with p15INK4b DNA methylation vs. samples with no DNA methylation AML clinical samples without DNA methylation exhibit bivalent histone modifications at p15INK4b, while clinical samples with DNA methylation display lower H3K4me3 and retain H3K27me3 Comparison of AML cell lines and clinical samples with p15INK4b DNA methylation to those free of DNA methylation. AML cell lines KG-1, KG-1a Kasumi-1, AML-193 have p15INK4b DNA methylation. AML patient samples AML6, AML7, AML8 have p15INK4b DNA methylation.
2010-05-06 | E-GEOD-16730 | biostudies-arrayexpress
Project description:Human myelopoiesis is an exciting biological model for cellular differentiation since it represents a plastic process where pluripotent stem cells gradually limit their differentiation potential, generating different precursor cells which finally evolve into distinct terminally differentiated cells. This study aimed at investigating the genomic expression during myeloid differentiation through a computational approach that integrates gene expression profiles with functional information and genome organization. The genomic distribution of myelopoiesis genes was investigated integrating transcriptional and functional characteristics of genes. The analysis of genomic expression during human myelopoiesis using an integrative computational approach allowed discovering important relationships between genomic position, biological function and expression patterns and highlighting chromatin domains, including genes with coordinated expression and lineage-specific functions. Keywords: cell differentiation Gene expression data from 20 experiments for 8 different cell types of the human myelopoietic lineage were used to generate an integrated myelopoiesis dataset.
2008-12-10 | E-GEOD-12803 | biostudies-arrayexpress
Project description:Dendritic Cell differentiation - CD molecule cluster follow up: The data files associated to this experiment show the gene expression levels for a subset of 152 transcripts (out of 12626 genes represented on Affymetrix Genechip HG_U95Av2) representing CD molecules specifically expressed in Dendritic Cells (DC) as assessed by the 9 conditions tested. Another subset of genes, corresponding to a cluster of Transcription regulators is available from E-MEXP-2 experiment.
2014-06-23 | E-MEXP-1 | biostudies-arrayexpress
Project description:Analysis of lin-CD34+CD45+ (iCD34+) cell population from two normal bone marrow-derived (BM1K and BM9) iPSCs and two CML (CML15 and CML17) iPSCs . CML iCD34+ cells have characteristics similar to primary CML leukemia stem cell in patients. Results provide insight into molecular profile characterized CML iCD34 and mechanism of its maintenance and drug resistance. iCD34+ cell samples obtained from two control BM1K and BM9 iPSCs (both for the same normal donor) and CML15 and CML17 iPSCs (both from the same patient in chronic phase of CML). Each group was treated with DMSO (control) or 5 μM imatinib. The complete phenotype for iCD34+ cells: lin-CD34+CD45+CD90+CD117+CD45RA-. This population also inclyde Rhodaminelow and ALDKhigh cells.
2014-08-31 | E-GEOD-60065 | biostudies-arrayexpress
Project description:Defining the role of epigenetic regulators in normal hematopoiesis has become critically important, as recurrent mutations or aberrant expression of these genes has been identified in both myeloid and lymphoid hematological malignancies. We have found that PRMT4, a type I arginine methyltransferase, whose function in normal and malignant hematopoiesis is unknown, is overexpressed in AML patient samples. In support of an oncogenic role for PRMT4, we find that its overexpression blocks the myeloid differentiation of human stem/progenitor cells (HSPCs) while its knockdown (KD) is sufficient to induce myeloid differentiation of HSPCs and multiple AML cell lines. Although classically thought of as a co-activator, we found that PRMT4 functions to repress the expression of miR-223 in HSPCs via the methylation of RUNX1, which triggers the assembly of a multi-protein repressor complex that includes DPF2. As part of a feedback loop, PRMT4 expression is repressed post-transcriptionally by miR-223 during the normal differentiation process. These data reveal an unidentified role of PRMT4 in myeloid differentiation and its unexpected repressive role in transcriptional regulation. Furthermore, depletion of PRMT4 results in the differentiation of myeloid leukemia cells in vitro and their decrease proliferation in vivo. Thus, targeting PRMT4 holds potential as a novel therapy for acute myelogenous leukemia. Purified human primary CD34+ cells were transduced with lentiviruses carrying PRMT4KD or scramble control shRNAs. Total RNA was extrated. RNAseq was performed to identify target genes that are regulated by PRMT4. Experiments were performed in triplicate.
2013-12-19 | E-GEOD-46056 | biostudies-arrayexpress
Project description:The current study investigated the effect of RAS-induced ROS production on gene expression in normal human haematopoietic progenitor cells (HPC) using gene expression profiling (GEP) and assessed whether ROS-induced gene expression changes contributed to the pro-proliferative phenotype. In order to determine the ROS-specific GEP, Affymetrix Human Exon 1.0ST arrays were used for the comparison of mutant RAS and control cells cultured in the presence or absence of the NOX inhibitor, DPI, which strongly suppressed the production of ROS.
2015-11-30 | E-MTAB-3551 | biostudies-arrayexpress