Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Cell-cell interactome of the hematopoietic niche and its changes in acute myeloid leukemia

ABSTRACT: Cell-cell interactome of the hematopoietic niche and its changes in acute myeloid leukemia

PROVIDER: PRJNA947256 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23934300_1.fastq.gz	Fastqsanger.gz
	SRR23934300_2.fastq.gz	Fastqsanger.gz
	SRR23934400_1.fastq.gz	Fastqsanger.gz
	SRR23934400_2.fastq.gz	Fastqsanger.gz
	SRR23934500_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 624

Similar Datasets

Comprehensive Analysis of Hematopoietic Stem Cell Niche

Project description:Comprehensive Analysis of Hematopoietic Stem Cell Niche

| PRJEB7266 | ENA

Synergistic, context-dependent and hierarchical functions of hematopoietic progenitor niche components.

Project description:Specialized niche environments specify and maintain stem and progenitor cells, but little is known about the identities and functional interactions of niche components in vivo. Here, we describe a modular system for the generation of artificial hematopoietic niches in the mouse embryo. A circumscribed tissue that lacks niche function but is physiologically accessible for hematopoietic progenitor cells is functionalized by individual and combinatorial expression of four factors, the chemokines Ccl25 and Cxcl12, the cytokine Scf and the Notch ligand DLL4. The distinct phenotypes and variable numbers of hematopoietic cells in the resulting niches reveal synergistic, context-dependent and hierarchical interactions among niche effector molecules. The surprisingly simple rules determining niche outcomes enable the in vivo engineering of artificial niches conducive to the presence of distinct myeloid or T or B lymphoid lineage precursors. The dataset comprises 24 samples divided into eight sample groups each representing a different lymphoid progenitor cell type isolated from wild-type (+/-) or transgenic (-/-) thymic niches. -/-, Foxn1-deficient genotype; +/-, Foxn1 heterozygous phenotype; DP, CD4/CD8 double-poisztive thymocytes; DN3, CD4/CD8-negative stage 3 thymocytes; SP4, CD4 single-positive thymocytes; SP8, CD8 single-positive thymocytes; B IgM-, IgM surface negative B cells; B IgM+, IgM surface positive B cells; B IgM- -/-, IgM surface negative B cells from Foxn1-deficient genotype.

2012-08-24 | E-GEOD-33268 | biostudies-arrayexpress

Breast cancer remotely imposes a myeloid bias on hematopoietic stem cells by reprogramming the bone marrow niche

Project description:Increased number of circulating myeloid cells is a hallmark of several cancers, however it remains unclear how primary tumors impact on myelopoiesis. Here we show that non-metastatic breast tumors remotely instruct the fate of long-term hematopoietic stem cell (HSCLT) in the bone marrow. We found that HSCLT from tumor bearing mice acquire a myeloid bias persisting upon primary and secondary HSCLT transfer in lethally-irradiated tumor-free animals. By imaging the bone marrow HSC niche, we found that the tumor-bearing status is associated with increased physical interactions between mesenchymal stem/stromal cells (MSC) and HSCLT. Moreover, ex vivo co-culture experiments demonstrate that MSC isolated from tumor-bearing mice increase myeloid differentiation of HSCLT isolated from tumor free mice. In summary, our data reveal that breast cancer remotely promotes myelopoiesis at the earliest stages of hematopoietic differentiation in the bone marrow mesenchymal niche.

2023-09-30 | GSE243964 | GEO

Cell-cell interactome of the hematopoietic niche and its changes in acute myeloid leukemia.

Project description:The bone marrow (BM) is a complex microenvironment, coordinating the production of billions of blood cells every day. Despite its essential role and its relevance to hematopoietic diseases, this environment remains poorly characterized. Here we present a high-resolution characterization of the niche in health and acute myeloid leukemia (AML) by establishing a single-cell gene expression database of 339,381 BM cells. We found significant changes in cell type proportions and gene expression in AML, indicating that the entire niche is disrupted. We then predicted interactions between hematopoietic stem and progenitor cells (HSPCs) and other BM cell types, revealing a remarkable expansion of predicted interactions in AML that promote HSPC-cell adhesion, immunosuppression, and cytokine signaling. In particular, predicted interactions involving transforming growth factor β1 (TGFB1) become widespread, and we show that this can drive AML cell quiescence in vitro. Our results highlight potential mechanisms of enhanced AML-HSPC competitiveness and a skewed microenvironment, fostering AML growth.

| S-EPMC10275994 | biostudies-literature

Cell-cell interactome of the hematopoietic niche and its changes in acute myeloid leukemia

Project description:Acute myeloid leukemia (AML) is an aggressive cancer which causes the rapid proliferation of immature myeloid-lineage blood cells (myeloblasts) in the bone marrow. These leukemic cells receive trophic signals from the bone marrow micro-environment (BMM) in which they reside, that are essential to the initiation and maintenance of the disease. Because this is a complex and heterogeneous tissue, many aspects of this environment remain poorly characterised due to experimental hurdles. Here we performed single-cell RNA-sequencing of bone marrow aspirates from 10 AML patients across multiple key timepoints in disease progression (diagnosis, post-treatment, relapse).

2023-06-13 | GSE227903 | GEO

Cardiovascular disease perturbs the vascular hematopoietic stem cell niche

Project description:Hematopoiesis advances cardiovascular disease by generating inflammatory leukocytes that attack the arteries, heart and brain. While it is well documented that the bone marrow niche regulates hematopoietic stem cell proliferation and hence the systemic leukocyte pool, it is less clear how cardiovascular disease affects the vasculature forming this niche. Here we show that arterial hypertension, atherosclerosis and myocardial infarction alter the anatomy and function of bone marrow vasculature. Hypertension and atherosclerosis instigated vascular fibrosis, leakage and endothelial dysfunction in the bone marrow. Myocardial infarction induced vascular leakage and bone marrow angiogenesis via Vegf signaling. Endothelial cell-specific deletion of the Vegf receptor 2 limited emergency hematopoiesis after myocardial infarction, indicating that new vasculature supports higher blood cell production. RNA-sequencing of bone marrow endothelial cells revealed inflammatory gene expression in mice with cardiovascular disease. Endothelial cell-specific deletion of interleukin 6 or versican, which were highly expressed in mice with atherosclerosis or myocardial infarction, respectively, reduced hematopoiesis and systemic myeloid cells. Taken together, cardiovascular disease affects the vascular bone marrow niche, thus influencing hematopoietic stem cell behavior and expanding innate immune cell supply to atherosclerotic plaque and ischemic myocardium. Interrupting this feed back loop may constrain cardiovascular inflammation.

2021-09-27 | GSE144498 | GEO

Stromal STAT5-mediated trophic activity regulates hematopoietic multipotent progenitor niche factors

Project description:Signal transducer and activator of transcription 5 (STAT5a and STAT5b) are intrinsically critical for normal hematopoiesis but are also expressed in stromal cells. However, hematopoiesis-supporting stromal function has not been reported. Here, STAT5ab knockout (KO) was generated with a variety of bone marrow hematopoietic and stromal Cre transgenic mouse strains. Pan-hematopoietic deletion with Vav1-Cre was the positive control for loss of multipotent hematopoietic function but surprisingly dysregulated niche factor mRNA expression and deleted STAT5ab in CD45neg cells. Single cell transcriptome analysis of mouse bone marrow from wild-type or Vav1-Cre KO mice showed major changes in hematopoietic stem cell myeloid commitment genes and upregulated protein translation genes throughout myeloid-primed clusters.

2023-10-01 | GSE214857 | GEO

Synergistic, context-dependent and hierarchical functions of hematopoietic progenitor niche components.

2012-08-24 | GSE33268 | GEO

Molecular analysis of the subaortic hematopoietic stem cell niche

Project description:Molecular analysis of the subaortic hematopoietic stem cell niche

| PRJNA669831 | ENA

Bmi1 suppresses adipogenesis in the hematopoietic stem cell niche

Project description:Bmi1 suppresses adipogenesis in the hematopoietic stem cell niche

| PRJNA496529 | ENA