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ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

ABSTRACT: ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

PROVIDER: PRJEB48618 | ENA |

REPOSITORIES: ENA

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ChIP-seq of EGR1 in human primary unstimulated monocytes and in unstimulated human monocytes from three CMML patients

Project description:Identification of EGR1 chromatin localization in human primary monocytes (2 donors), in human primary monocytes from 2 CMML patients with TET2 truncating mutations (high VAF) and in human primary monocytes from 1 CMML patients with TET2 truncating mutations with low VAF.

2021-11-15 | E-MTAB-11132 | biostudies-arrayexpress

ChIP-seq of CSF-1R, H3K4me1, H3K4me3 in human primary unstimulated monocytes and monocytes differentiated 72h with CSF-1 (3 healthy donors buffy coat) and in monocytes from two CMML patients and one healthy donor, EGR1 ChIP-seq in unstimulated monocytes (3 healthy donors buffy coat)

Project description:Identification of nuclear CSF-1R, H3K4me1 and H3K4me3 localization on chromatin in human primary monocytes and modification of this localization during monocyte differentiation into macrophage induced by 100ng/mL CSF-1 during 6 hours (1 donor) or 72h (3 donors). Identification of EGR1 chromatin localization in human primary monocytes (3 donors) Comparison of nuclear CSF-1R chromatin localization in monocytes from 1 healthy donor and 2 chronic myelomonocytic leukemia patients.

2019-03-04 | E-MTAB-6305 | biostudies-arrayexpress

ChIP-seq of CSF-1R in THP-1 cell lines deleted for EGR1 gene by CRISPR-Cas9 and ChIP-seq of CSF-1R in 2 CMML patients

Project description:CSF-1R is recruited on EGR1 motifs in monocytes where it colocalizes with EGR1. To address if EGR1 required for CSF-1R recruitment on chromatin, THP-1 monocytic cell line has been deleted for EGR1 by CRISPR-Cas9 approach. 3 clones were generated by single cell cloning and CSF-1R localization on chromatin was compared to two unmodified THP-1 clones by ChIP-sequencing. Since the read number was strongly decreased in the EGR1-deleted clones, the three clones were pooled for the comparison with wild-type clones. ChIPseq of CSF-1R (Nter Antibody) in monocytes of two CMML patients (CMML2130 and CMML2609)

2019-03-28 | E-MTAB-7756 | biostudies-arrayexpress

Project description:ChIP-seq of CSF-1R, H3K4me1, H3K4me3 in human primary unstimulated monocytes and monocytes differentiated 72h with CSF-1 (3 healthy donors buffy coat) and in monocytes from two CMML patients and one healthy donor, EGR1 ChIP-seq in unstimulated monocytes (3 healthy donors buffy coat)

| PRJEB23999 | ENA

The Transcriptome Of Cmml Monocytes Is Highly Inflammatory And Reflects Leukemia-Specific And Age-Related Alterations

Project description:Chronic myelomonocytic leukemia (CMML) is an aggressive myeloid neoplasm of older individuals characterized by persistent monocytosis. Somatic mutations in CMML are heterogeneous and only partially explain the variability in clinical outcomes. Recent data suggest that cardiovascular morbidity is increased in CMML and contributes to reduced survival. Clonal hematopoiesis of indeterminate potential (CHIP), the presence of mutated blood cells in hematologically normal individuals, is a precursor of age-related myeloid neoplasms and associated with increased cardiovascular risk. To isolate CMML-specific alterations from those related to aging, we performed RNA sequencing and DNA methylation profiling on purified monocytes from CMML patients and from age-matched (old) and young healthy controls. We found that the transcriptional signature of CMML monocytes is highly pro-inflammatory, with upregulation of multiple inflammatory pathways, including tumor necrosis factor, IL-6 and IL-17 signaling, while age per se does not significantly contribute to this pattern. We observed no consistent correlations between aberrant gene expression and CpG island methylation, suggesting that pro-inflammatory signaling in CMML monocytes is governed by multiple and complex regulatory mechanisms. We propose that pro-inflammatory monocytes may contribute to cardiovascular morbidity in CMML patients, and promote progression by selection of mutated cell clones. Our data raise questions whether asymptomatic CMML patients may benefit from monocyte-depleting or anti-inflammatory therapies.

2019-10-24 | GSE135902 | GEO

Expression data from Annexin A1 Ac1-25 vs. Unstimulated human peripheral blood monocytes

Project description:We used microarrays to detail the global gene expression changes elicited by stimulation of human peripheral blood monocytes from buffy coats with 50µM Annexin A1 peptide Ac1-25 for 2h versus unstimulated control monocytes. Keywords: comparative gene expression study

2007-09-19 | GSE9080 | GEO

Macrophage migration inhibitory factor is overproduced through EGR1 in TET2low resting monocytes

Project description:Somatic mutation in TET2 gene is one of the most common clonal genetic events detected in age-related clonal hematopoiesis as well as in chronic myelomonocytic leukemia (CMML). In addition to being a pre-malignant state, TET2 mutated clones are associated with an increased risk of death from cardiovascular disease, which could involve cytokine/chemokine overproduction by monocytic cells. Here, we show in mice and in human cells that, in the absence of any inflammatory challenge, TET2 down-regulation promotes the production of MIF (macrophage migration inhibitory factor), a pivotal mediator of atherosclerotic lesion formation. In healthy monocytes, TET2 is recruited to MIF promoter and interacts with the transcription factor EGR1 and histone deacetylases. Disruption of these interactions as a consequence of TET2-decreased expression favors EGR1-driven transcription of MIF gene and its secretion. MIF favors monocytic differentiation of myeloid progenitors. These results designate MIF as a chronically overproduced chemokine and a potential therapeutic target in patients with clonal TET2 down-regulation in myeloid cells.

2021-11-13 | GSE188624 | GEO

Human periheral blood-derived monocytes and unstimulated as well as IL-4-stimulated differentiating macrophages

Project description:CD14+ monocytes were separated from human peripheral blood and exposed to IL-4 for 12 or 72 hours then subjected to microarray analysis We used Affymetrix miRNA1.0 microarray to obtain global miRNA expression data of human monocytes, unstimulated and IL-4-stimulated differentiating macrophages.

2016-04-29 | GSE71641 | GEO

ChiP-seq of H3K4me3 in primary unstimulated monocytes from 3 healthy donors buffy coats and from 4 CMML patients

Project description:Identification of H3K4me3 localization on chromatin in primary unstimulated monocytes

2018-11-09 | E-MTAB-6689 | biostudies-arrayexpress

Cytokine-like protein 1-induced survival of monocytes suggests a combined strategy targeting MCL1 and MAPK in CMML [RNA-Seq]

Project description:Mouse models of chronic myeloid malignancies suggest that targeting mature cells of the malignant clone disrupts feedback loops that promote disease expansion. Here, we show that, in chronic myelomonocytic leukemia (CMML), monocytes that accumulate in the peripheral blood show a decreased propensity to die by apoptosis. BH3 profiling demonstrates their addiction to MCL1 (myeloid cell leukemia-1), which can be targeted with the small molecule inhibitor S63845. RNA sequencing and DNA methylation pattern analysis both point also to the implication of the MAPK (mitogen-activated protein kinase) pathway in the resistance of CMML monocytes to death and reveal an autocrine pathway in which the secreted cytokine CYTL1 (Cytokine-like protein 1) promotes ERK (extracellular signal-regulated kinase) activation through CCR2 (C-C chemokine receptor type 2). Combined MAPK and MCL1 inhibition restores apoptosis of CMML patient monocytes and reduces the expansion of patient-derived xenografts in mice. These results designate the combined inhibition of MCL1 and MAPK as a promising approach to slow down CMML progression by inducing leukemic monocyte apoptosis.

2021-01-23 | GSE165304 | GEO

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