Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA197142 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Human bone marrow mesenchymal stromal cells (BM-MSC) could be committed toward a functional lymphoid-like stroma by a combination of TNFalpha (TNF) and Lymphotoxin alpha1/beta2 (LT) (Amé-Thomas et al Blood 2007). Bone marrow and lymph node stromal cells support FL malignant cell recruitment and growth in particular after comittment to a lymphoid-like differentiation in vitro. In addition, more than 70% of FL patients exhibit a bone marrow involvment at diagnosis. We delineate using Affymetrix U133+2.0 microarrays the gene expression profile of BM-MSC obtained from FL patients (FL-MSC) and age-matched healthy donors (HD-MSC) in order to identify a specific FL-MSC signature. In addition, we used Affymetrix microarrays to define the gene expression signature of lymphoid-like stromal cells obtained from HD-MSC by treatment with TNF/LT in vitro. This TNF/LT signature was then used to interpret the gene expression profile of FL-MSC. GEP was performed on 10 BM-MSC from FL patients and 6 from healthy donors, treated or not with TNF(10 ng/mL)/LT(100ng/mL)
2012-01-26 | E-GEOD-35331 | biostudies-arrayexpress
Project description:Human bone marrow mesenchymal stromal cells (BM-MSC) could be committed toward a functional lymphoid-like stroma by a combination of TNFalpha (TNF) and Lymphotoxin alpha1/beta2 (LT) (Amé-Thomas et al Blood 2007). Bone marrow and lymph node stromal cells support FL malignant cell recruitment and growth in particular after comittment to a lymphoid-like differentiation in vitro. In addition, more than 70% of FL patients exhibit a bone marrow involvment at diagnosis. We delineate using Affymetrix U133+2.0 microarrays the gene expression profile of BM-MSC obtained from FL patients (FL-MSC) and age-matched healthy donors (HD-MSC) in order to identify a specific FL-MSC signature. In addition, we used Affymetrix microarrays to define the gene expression signature of lymphoid-like stromal cells obtained from HD-MSC by treatment with TNF/LT in vitro. This TNF/LT signature was then used to interpret the gene expression profile of FL-MSC.
2012-01-26 | GSE35331 | GEO
Project description:Expression analysis of migrating and non-migrating mesenchymal stromal cells (MSC) in fetal bone marrow Keywords: fetal bone marrow, mesenchymal stromal cells, migration, gene expression, genomics Three biological replates for both migrating and non-migrating mesenchymal stromal cells (MSC) in fetal bone marrow
2011-10-23 | E-GEOD-24892 | biostudies-arrayexpress
Project description:Bone marrow (BM) niches provide an optimal substrate for multiple myeloma (MM) cell lodgement and growth. Nevertheless, little is known about the putative mechanisms by which the BM microenvironment can lead to initiation or progression of oncogenesis in this disease. We have demonstrated that BM mesenchymal stromal cell-derived exosomes transfer their miRNA and protein content to clonal plasma cells, thus acting as synaptic vesicles responsible for molding the microenvironment surrounding multiple myeloma (MM) cells, leading to MM growth, dissemination and, therefore, disease progression. We used microarray to detail the changes in microRNA expression in MM-BM mesenchymal stromal cell (MSC)-derived exosomes, compared to normal- and monoclonal gammopathy of undetermined significance- BM-MSC-derived exosomes.
2013-07-24 | GSE39571 | GEO
Project description:The myeloma bone marrow microenvironment drives proliferation of malignant plasma cells and promotes resistance to therapy. Interleukin-6 (IL-6) and downstream JAK/STAT signaling are thought to be central components of these microenvironment-induced phenotypes. In a prior drug repurposing screen, we identified tofacitinib, a pan-JAK inhibitor FDA-approved for rheumatoid arthritis, as an agent that may reverse the tumor-stimulating effects of bone marrow mesenchymal stromal cells.Here, we validated both in vitro, in stromal-responsive human myeloma cell lines, and in vivo, in orthotopic disseminated murine xenograft models of myeloma, that tofacitinib showed both single-agent and combination therapeutic efficacy in myeloma models. Surprisingly, we found that ruxolitinib, an FDA-approved agent targeting JAK1 and JAK2, did not lead to the same anti-myeloma effects. Combination with a novel irreversible JAK3-selective inhibitor also did not rescue ruxolitinib effects. RNA-seq and unbiased phosphoproteomics revealed that marrow stromal cells drive a JAK/STAT-mediated proliferative program in myeloma plasma cells, and tofacitinib reversed the large majority of these pro-growth signals. Taken together, our results suggest that tofacitinib specifically reverses the growth-promoting effects of the tumor microenvironment through blocking an IL-6-mediated signaling axis. As tofacitinib is already FDA-approved, these results can be rapidly translated into potential clinical benefits for myeloma patients.
2018-10-24 | PXD006581 | Pride
Project description:We have analysed tes adipocytic, osteoblastic, chondrocytic and vascular smooth muscle differentiation of the stromal potential of 5 mouse mesenchymal lines derived from hematopoietic sites (bone marrow and fetal liver). The sole line, AFT024, that provide both quadripoential and capable of maintening hematopoiesis in vitro, has served as reference for genomic studies aimed at establishing the signature of the multipotential stromal mesenchymal stem cell (MSC). Keywords: molecular signature of MSC
2006-07-01 | GSE4491 | GEO
Project description:Expression analysis of migrating and non-migrating mesenchymal stromal cells (MSC) in fetal bone marrow Keywords: fetal bone marrow, mesenchymal stromal cells, migration, gene expression, genomics
2011-10-24 | GSE24892 | GEO
Project description:Bone marrow (BM) niches provide an optimal substrate for multiple myeloma (MM) cell lodgement and growth. Nevertheless, little is known about the putative mechanisms by which the BM microenvironment can lead to initiation or progression of oncogenesis in this disease. We have demonstrated that BM mesenchymal stromal cell-derived exosomes transfer their miRNA and protein content to clonal plasma cells, thus acting as synaptic vesicles responsible for molding the microenvironment surrounding multiple myeloma (MM) cells, leading to MM growth, dissemination and, therefore, disease progression. We used microarray to detail the changes in microRNA expression in MM-BM mesenchymal stromal cell (MSC)-derived exosomes, compared to normal- and monoclonal gammopathy of undetermined significance- BM-MSC-derived exosomes. Exosomes have been isolated from cell culture supernatant of BM-MSCs (MM=7; MGUS=2; Normal=4), and subsequently evaluated at ultrastructural level by using electron microscopy and immunogolf labeling. RNA was extracted; and miRNA profiling has been assessed by using TaqMan human miRNA profiling. Mean miRNA expression value has been used for miRNA RT-qPCR data normalization, as described (Mestdagh et al., 2009).
2013-07-24 | E-GEOD-39571 | biostudies-arrayexpress
Project description:Purpose: In this study we compared bone marrow-derived mesenchymal stem cells (MSC) of 6 Multiple Myeloma patients (MM-MSC) with MSC of 5 control donors with other (non) malignant diseases (CTR-MSC) to detect transciptomic alterations in RNA sequencing and to identify altered gene expression patterns. Methods: MSC were obtained from bone marrow, cultivated, analyzed by flow cytometry and underwent quality control using the 4200 TapeStation (Agilent, California, USA). Following the TrueSeq stranded protocol (Illumina, California, USA) we sequenced the RNA in a 100 bp paired-end run on the HiSeq 4000 (Illumina). Results: We detected 2174 significant DEGs (adjusted p<0.05) between MM-MSC and CTR-MSC, among which 967 were up-regulated in MM-MSC. 18 out of 50 MSigDB Hallmark gene sets were significantly enriched in MM-Act-MSC compared to CTR-MSC (FDR<0.05) including PI3K-AKT-mTOR signaling, as well as NOTCH, MYC and Inflammatory response. Conclusion: Our data provides a deeper insight into the molecular signature and function of MSC associated MM-cells and show that targeting PI3K-AKT-mTOR signaling in MSC may represent an additional therapeutic pathway in the treatment of MM-patients.
2022-05-13 | GSE196297 | GEO
Project description:Mesenchymal stromal cells (MSCs) are multipotent progenitors supporting bone marrow hematopoiesis. MSC have an efficient DNA damage response (DDR) and are consequently reatively radio-resistant cells. Therefore, MSCs are key to hematopoietic reconstitution following total body irradiation (TBI) and bone marrow transplantation (BMT). The bone marrow niche is hypoxic and via the heterodimeric transcription factor Hypoxia-inducible factor-1 (Hif-1), hypoxia enhances the DDR. Using gene knock-down, we have previously shown that the Hif-1α subunit of Hif is involved in MSC radio-resistance, however its exact mechanism of action remains unknown. In order to dissect the involvement of Hif-1α in the DDR, we have generated using CRISPR/Cas9 technology, a stable MS5 mouse MSC cell line lacking Hif-1 expression. Herein, we show that it is the whole Hif-1 transcription factor, and not only the Hif-1α subunit, that modulates the DDR of mouse MSCs, and that this effect is dependent upon the integrity of the DNA binding domain. We have also characterized the Hif-1α-dependent proteomic changes undergone by hypoxic MS5 cells. These findings have important implications for the modulation of MSC radio-resistance in the context of BMT and cancer.
2018-05-16 | PXD006701 | Pride