Gene expression data of bone marrow mesenchymal stromal cells in myelofibrosis
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE84387 | GEO | 2017/03/31
SECONDARY ACCESSION(S): PRJNA329045
REPOSITORIES: GEO
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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
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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 neoangiogenesis and an osteosclerosis concomitant to the myeloproliferation and to the increase number of circulating hematopoietic progenitors suggests that the crosstalk between hematopoietic and stromal cells is deregulated in the PMF BM microenvironment. Within these niches, Mesenchymal Stromal Cells (BM-MSC) play a supportive role in the production of growth factors and extracellular matrix which regulate the proliferation, differentiation, adhesion and migration of hematopoietic progenitors. A transcriptome analysis of BM-MSC in PMF patients will help to characterize their molecular alterations and to understand their involvement in the hematopoietic progenitor deregulation that features PMF. Primary Myelofibrosis, mesenchymal stroma cells, bone marrow, myeloproliferative disorders Transcriptome analysis was performed on BM-MSC amplified in vitro after 3 to 5 passages. Agilent Whole Human Genome Oligo Microarrays were used to compare expression profiling of BM-MSC from PMF patients and healthy donors.
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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.
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Project description:Myelofibrosis (MF) is a progressive, bone marrow (BM) malignancy associated with monocytosis, and is believed to promote the pathological remodelling of the extracellular matrix. Here, we show that the pathologic grading of MF was associated with inflammatory gene expression in primary patient samples.
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Project description:Adult hematopoietic stem cells (HSCs) reside primarily in bone marrow. However, hematopoietic stresses such as myelofibrosis, anemia, pregnancy, infection or myeloablation can mobilize HSCs to the spleen and induce extramedullary hematopoiesis (EMH). While the bone marrow HSC niche has been studied intensively, the EMH niche has received little attention. Here, we systematically assessed the physiological sources of the key niche factors, SCF and CXCL12, in the mouse spleen after EMH induction by cyclophosphamide plus granulocyte colony-stimulating factor, blood loss, or pregnancy. In each case, Scf was expressed by endothelial cells and Tcf21+ stromal cells, primarily around sinusoids in red pulp, while Cxcl12 was expressed by a subset of Tcf21+ stromal cells. EMH induction markedly expanded the Scf-expressing endothelial cells and stromal cells by inducing proliferation. Most splenic HSCs were adjacent to Tcf21+ stromal cells in red pulp. Conditional deletion of Scf from spleen endothelial cells or Scf or Cxcl12 from Tcf21+ stromal cells severely reduced spleen EMH and reduced blood cell counts without affecting bone marrow hematopoiesis. Endothelial cells and Tcf21+ stromal cells thus create the splenic EMH niche, which is necessary for the physiological response to diverse hematopoietic stresses.
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Project description:Fibrosis is the hallmark of primary myelofibrosis, a disease characterized by increased TGF-β bioavailability in bone marrow and spleen from both patients and mouse models. The aim of this study was to verify the role of TGF-β signaling in comparison to essential thrombocythemia and non-diseased control by using human bone marrow. We used RNA microarrays to investigate gene expression in bone marrow and identified distinct classes of up/down-regulated genes during this process.
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