Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Expression data from osteoblastic lineage cells isolated from normal and leukemic mice

ABSTRACT: Multipotent stromal cells (MSC) and their osteoblastic lineage cell (OBC) derivatives are part of the bone marrow (BM) niche and contribute to hematopoietic stem cell (HSC) maintenance. During myeloproliferative neoplasm (MPN) development, MSCs are stimulated to overproduce functtionally altered OBCs, which accumulate in the BM cavity as myelofibrotic cells. These MPN-expanded OBCs, in turn, impair the maintenance of normal HSCs but not of leukemic stem cells. We used microarrays to detail the global gene expression changes in OBCs during BCR/ABL-induced MPN development, and understand the molecular deregulations contributing to their functional changes.

ORGANISM(S): Mus musculus

PROVIDER: GSE48438 | GEO | 2013/07/11

SECONDARY ACCESSION(S): PRJNA210141

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Expression data from osteoblastic lineage cells isolated from normal and leukemic mice

Project description:Multipotent stromal cells (MSC) and their osteoblastic lineage cell (OBC) derivatives are part of the bone marrow (BM) niche and contribute to hematopoietic stem cell (HSC) maintenance. During myeloproliferative neoplasm (MPN) development, MSCs are stimulated to overproduce functtionally altered OBCs, which accumulate in the BM cavity as myelofibrotic cells. These MPN-expanded OBCs, in turn, impair the maintenance of normal HSCs but not of leukemic stem cells. We used microarrays to detail the global gene expression changes in OBCs during BCR/ABL-induced MPN development, and understand the molecular deregulations contributing to their functional changes. OBCs were isolated from diseased Scl-tTA::TRE-BCR/ABL (BA) mice and age-match controls around 5-6 weeks post-doxycycline withdrawal. Five independent biological replicate corresponding to single mice were used for each population. RNA was extracted, amplified and hybridized on Affymetrix Gene ST 1.0 microarrays.

2013-07-11 | E-GEOD-48438 | biostudies-arrayexpress

Transcriptome analysis of in vitro MSC-derived osteoblastic cells from patients with Primary Myelofibrosis

Project description:Primary myelofibrosis (PMF) is a clonal myeloproliferative neoplasm whose severity and treatment complexity is attributed to the presence of bone marrow (BM) fibrosis and alterations of stroma impairing the production of normal blood cells. Despite the recently discovered mutations including the JAK2V617F mutation in about half of patients, the primitive event responsible for the clonal proliferation is still unknown. In the highly inflammatory context of PMF, the presence of fibrosis associated with a neo-osteogenesis and an osteosclerosis concomitant to the myeloproliferation and to the increase number of circulating hematopoietic progenitors suggests that the crosstalk between hematopoietic cells and the osteoblastic niche is deregulated in the PMF BM microenvironment. Osteoblastic niche is well known to be an important support to regulate hematopoietic stem cell functions in bone marrow. A transcriptome analysis of bone marrow mesenchymal stem cells (BM-MSC) induced in vitro to differentiate in osteoblasts will help to understand the role of these cells in pathophysiology of PMF. Transcriptome analysis was performed on BM-MSC at J0 and J21 of in vitro osteoblastic differentiation. Agilent Whole Human Genome Oligo Microarrays were used to compare expression profiling of BM-MSCs from PMF patients and healthy donors before and after osteoblastic differentiation. Primary Myelofibrosis, mesenchymal stroma cells, bone marrow, myeloproliferative disorders

2015-01-10 | E-GEOD-46021 | biostudies-arrayexpress

Molecular reprogramming of granulocyte/macrophage progenitor (GMP) clusters upon induction of BCR/ABL oncogene

Project description:Single cell RNA Seq and bioinformatic analysis are used to study what processes are important for the molecular reprogramming of GMPs once mice develop chronic myelogenous leukemia-like (CML-like) myeloproliferative neoplasm (MPN) upon induction of BCR/ABL oncogene.

2017-03-31 | GSE90797 | GEO

Transcriptome analysis of in vitro MSC-derived osteoblastic cells from patients with Primary Myelofibrosis

2015-01-10 | GSE46021 | GEO

Project description:Sequencing of Myeloproliferative Neoplasm (MPN) Samples

| PRJNA754686 | ENA

Genomic_analysis_of_408_myeloproliferative neoplasm(MPN)_samples

Project description:Genomic DNA of granulocytes or mononuclear cell fractions of 408 myeloproliferative neoplasm (MPN) patients was analyzed using Affymetrix Genome-Wide Human SNP 6.0 arrays

2011-07-01 | E-MTAB-608 | biostudies-arrayexpress

Gene expression of MYB wild type and MYB knockdown myeloproliferative K11bL cells

Project description:Low levels of MYB promote the development of myeloproliferative neoplasm (MPN). The cell type identified that can transplant the MPN phenotype has been identified as expressing KIT, CD11b and low levels of lineage markers (K11bL). We sought to identify changes in gene expression between wild type and MYB knockdown K11bL cells to identify potential targets of MYB that play a role in the establishment of MPN.

2017-06-19 | GSE74140 | GEO

Haplodeficiency of the 9p21 Tumor Suppressor Locus Causes Myeloid Disorders Driven by Bone Marrow Microenvironment

Project description:The chromosome 9p21 locus comprises several tumor suppressor genes including MTAP, CDKN2A and CDKN2B, and its homo- or heterozygous deletions are associated with reduced survival in multiple cancer types. We report that mice with germline monoallelic deletion or induced biallelic deletion of the 9p21-syntenic locus (9p21s) developed fatal myelodysplastic syndrome/myeloproliferative neoplasm (MDS/MPN)-like disease associated with aberrant trabecular bone formation and/or fibrosis in the bone marrow (BM). Reciprocal BM transfers and conditional targeting of 9p21s suggested that the disease originates in the BM stroma. Single-cell analysis of 9p21s-deficient BM stroma revealed the expansion of chondrocyte and osteogenic precursors, reflected in increased osteogenic differentiation in vitro. It also showed reduced expression of factors maintaining hematopoietic stem/progenitor cells, including Cxcl12. Accordingly, 9p21s-deficient mice showed reduced levels of circulating Cxcl12 and a concomitant upregulation of the pro-fibrotic chemokine Cxcl13. Our study highlights the potential of mutations in the BM microenvironment to drive MDS/MPN-like disease. We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different cells at two time points.

2023-06-06 | GSE211779 | GEO

IL-1β promotes MPN disease initiation by favoring early clonal expansion of JAK2-mutant hematopoietic stem cells

Project description:JAK2-V617F is the most frequent somatic mutation causing myeloproliferative neoplasm (MPN). JAK2-V617F can be found in healthy individuals with clonal hematopoiesis of indeterminate potential (CHIP) with a frequency much higher than the prevalence of MPN. The factors controlling the conversion of JAK2-V617F CHIP to MPN are largely unknown. We hypothesized that IL-1β mediated inflammation can favor this progression. We established an experimental system using bone marrow (BM) transplantations from JAK2-V617F and GFP transgenic (VF;GFP) mice, that were further crossed with IL-1β-/- or IL-1R1-/- mice. To study the role of IL-1β and its receptor on monoclonal evolution of MPN, we performed competitive BM transplantations at high dilutions with only 1-3 hematopoietic stem cells (HSCs) per recipient. Loss of IL-1β in JAK2-mutant HSCs reduced engraftment, restricted clonal expansion, lowered the total numbers of functional HSCs, and decreased the rate of conversion to MPN. Loss of IL-1R1 in the recipients also lowered the conversion to MPN, but did not reduce the frequency of engraftment of JAK2-mutant HSCs. WT recipients transplanted with VF;GFP BM that developed MPN had elevated IL-1β levels and reduced frequencies of mesenchymal stromal cells (MSCs). Interestingly, frequencies of MSCs were also reduced in recipients that did not develop MPN, had only marginally elevated IL-1β levels and displayed low GFP-chimerism resembling CHIP. Anti-IL-1β antibody preserved high frequencies of MSCs in VF;GFP recipients and reduced the rate of engraftment and the conversion to MPN. Our results identify IL-1β as a potential therapeutic target for preventing the transition from JAK2-V617F CHIP to MPN.

2024-01-29 | GSE250507 | GEO

HMGA2 overexpression

Project description:Overexpression of high mobility group AT-hook 2 (HMGA2) associated with truncations of its 3’ untranslated region (UTR) with let-7 micro RNA-complementary sequences have been identified in patients with paroxysmal nocturnal hemoglobinuria (PNH). Here, we generated transgenic mice (∆Hmga2 mice) with a 3’UTR-trncated Hmga2 cDNA that overexpress Hmga2 mRNA and protein in hematopoietic organs. ∆Hmga2 mice showed proliferative hematopoiesis that mimicked a myeloproliferative neoplasm (MPN)-like phenotype with increased numbers of all lineages of peripheral blood cells, hypercellular bone marrow (BM), splenomegaly with extramedullary erythropoiesis, and erythropoietin-independent erythroid colony formation compared to wild-type mice. ∆Hmga2 BM-derived cells took over most of hematopoiesis in competitive repopulations during serial BM transplants. When we bred mice with circulating PNH cells (Piga- mice) with ∆Hmga2 mice, the lack of GPI-linked proteins did not add an additional clonal advantage to the ∆Hmga2+ cells. In summary, our results showed that the overexpression of a 3’UTR-truncated Hmga2 leads to a proliferative hematopoiesis with clonal advantage, which may explain clonal expansion in PNH or MPN at the level of HSC.

2011-02-06 | GSE24071 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data