Transcriptomics

Dataset Information

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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. 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.

REANALYSED by: E-GEOD-48438

ORGANISM(S): Mus musculus  

SUBMITTER: Pietras M Eric  Schepers Koen   Passegué Emmanuelle   Emmanuelle Passegué    

PROVIDER: E-GEOD-48438 | ArrayExpress | 2013-07-11

SECONDARY ACCESSION(S): GSE48438PRJNA210141

REPOSITORIES: GEO, ArrayExpress

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Publications

Myeloproliferative neoplasia remodels the endosteal bone marrow niche into a self-reinforcing leukemic niche.

Schepers Koen K   Pietras Eric M EM   Reynaud Damien D   Flach Johanna J   Binnewies Mikhail M   Garg Trit T   Wagers Amy J AJ   Hsiao Edward C EC   Passegué Emmanuelle E  

Cell stem cell 20130711 3


Multipotent stromal cells (MSCs) and their osteoblastic lineage cell (OBC) derivatives are part of the bone marrow (BM) niche and contribute to hematopoietic stem cell (HSC) maintenance. Here, we show that myeloproliferative neoplasia (MPN) progressively remodels the endosteal BM niche into a self-reinforcing leukemic niche that impairs normal hematopoiesis, favors leukemic stem cell (LSC) function, and contributes to BM fibrosis. We show that leukemic myeloid cells stimulate MSCs to overproduce  ...[more]

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