Ontology highlight
ABSTRACT:
PROVIDER: PRJEB39993 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR4496480_1.fastq.gz | Fastqsanger.gz | |||
| ERR4496480_2.fastq.gz | Fastqsanger.gz | |||
| ERR4496481_1.fastq.gz | Fastqsanger.gz | |||
| ERR4496481_2.fastq.gz | Fastqsanger.gz | |||
| ERR4496482_1.fastq.gz | Fastqsanger.gz |
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Project description:We isolated non-hematopoietic cells from fibrotic and non-fibrotic human bone marrow and perfomed scRNAseq on them. We identified 3 different stromal populations and 2 populations of hematopoietic progenitors. Our analysis revealed mesenchymal stromal cells (MSC) as pro-fibrotic cells. MSCs were functionally reprogrammed with loss of their progenitor status and acquisition of a pro-fibrotic phenotype in the fibrotic bone marrow. Additionally, stromal cells exhibited an upregulation of pro-inflammatory mediators like S100A8/A9.
2020-11-03 | GSE156640 | GEO
Project description:We isolated non-hematopoietic cells from fibrotic and non-fibrotic mouse bone marrow and perfomed scRNAseq on them. We identified 8 different stromal populations. Our analysis revealed two distinct mesenchymal stromal cells (MSC) subsets as pro-fibrotic cells. MSCs were functionally reprogrammed in a stagedependent manner with loss of their progenitor status and initiation of differentiation in the prefibrotic stage and acquisition of a pro-fibrotic and inflammatory phenotype in the fibrotic stage. In parallel, IL-33-expressing myelinating Schwann cell progenitors expanded, likely as a repair mechanism for the previously described neuropathy in MPN.
2020-11-03 | GSE141736 | GEO
Project description:Neutrophils are the most abundant nucleated cell type in the bone marrow. A pro-tumor bias in this cell type may have implications for bone-marrow residing malignancies, such as multiple myeloma. Here, we generated single cell transcriptomic overviews of the entire myeloid compartment, including the entire neutrophilic lineage, of the bone marrow of 6 newly diagnosed myeloma patients, 5 treated myeloma patients and 4 non-cancer controls. We find dat mature neutrophils in myeloma patients, both newly diagnosed and treated, have an activated and pro-inflammatory phenotype, accompanied by increased transcription of pro-inflammatory cytokines, such as IL-1β, and myeloma cell survival factors, such as BCMA-ligand BAFF/TNFSF13B. Moreover, inflammatory stromal cells can activate naive neutrophils to acquire an inflammatory phenotype as is seen in patients. Previously, we have shown that inflammatory stromal cells characterized the bone marrow of newly diagnosed myeloma patients. Here, we generate single cell RNA sequencing dataset of non-hematopoietic bone marrow cells of patients after induction treatment, high-dose melphalan, stem cell transplantation and consolidation treatment. We show that this intensive treatment reduced, but did not normalize, stromal inflammation.
2023-03-31 | E-MTAB-12760 | biostudies-arrayexpress
Project description:Hypertension and persistent activation of the renin-angiotensin system (RAS) are predisposing factors for development of acute kidney injury (AKI). Although bone marrow-derived stromal cells (BMSCs) have shown therapeutic promise in treatment of AKI, the impact of pathological RAS on BMSC functionality has remained unresolved. RAS and its local components in the bone marrow are involved in several key steps of cell maturation processes. This may also render BMSC population vulnerable to alterations even in the early phases of RAS pathology. We isolated TG-BMSCs from young, end organ disease-free rats with increased RAS activation (human angiotensinogen/renin double transgenic rats; dTGR) that eventually develop hypertension and die of end-organ damage and kidney failure at 8-weeks-of-age. Control cells were isolated from wild-type Sprague-Dawley rats (SD-BMSCs). Cell phenotype, mitochondrial reactive oxygen species (ROS) production and respiration were assessed, and gene expression profiling was carried out using microarrays. Cells’ therapeutic efficacy was evaluated in a rat model of acute ischemia-reperfusion-induced AKI. Serum urea and creatinine were measured at 24h and 48h. Acute tubular damage was scored and immunohistochemistry was used for evaluation for markers of inflammation (MCP-1, ED-1), and kidney injury (KIM-1, NGAL). TG-BMSCs showed distinct mitochondrial morphology, decreased cell respiration, and increased production of ROS. Gene expression profiling revealed a pronounced pro-inflammatory phenotype. In contrast to the therapeutic effect of SD-BMSCs, administration of TG-BMSCs in the AKI model resulted in exacerbation of kidney injury and high mortality. Our results demonstrate that early persistent RAS activation can dramatically compromise therapeutic potential of BMSCs by shift into a pro-inflammatory phenotype with mitochondrial dysfunction. A comparison of transcriptome of a bone marrow-derived stromal cells from a double-transgene rats compared to those from control rats
2014-03-31 | E-GEOD-51593 | biostudies-arrayexpress
Project description:Leukemia Cell Lines Induce Changes in Bone Marrow Stromal Cells
| PRJNA195933 | ENA
Project description:To investigate the alteration of bone marrow environment caused by Pinch loss, we performed single-cell RNA-sequencing on bone marrow cells, including hematopoietic cells and non-hematopietic stromal cells. As results indicated, we found both cell type proportion and transcriptomic signatures were dramatically altered by Pinch loss. We identified genes related to ossification, extracellular matrix organization, skeletal system development, and vasculature structure development were significantly differentially expressed between control group and dKO group in many mesenchymal stromal cells. Our results revealed Pinch loss disrupted homeostasis of bone marrow niche, monocytes in bone marrow were actively involved in inflammatory response, and functions of mesenchymal stromal cells was severely disrupted.
2023-12-08 | GSE152217 | GEO
Project description:Dyskeratosis congenita (DC) is an inherited multi-system disorder, characterized by oral leukoplakia, nail dystrophy, and abnormal skin pigmentation, as well as high rates of bone marrow failure, solid tumors, and other medical problems such as osteopenia. DC and telomere biology disorders (collectively referred to as TBD here) are caused by germline mutations in telomere biology genes leading to very short telomeres and limited proliferative potential of hematopoietic stem cells. We found that skeletal stem cells (SSCs) within the bone marrow stromal cell population (BMSCs, also known as bone marrow-derived mesenchymal stem cells), may contribute to the hematological phenotype. TBD-BMSCs exhibited reduced clonogenicity, reduced telomerase activity, spontaneous differentiation into adipocytes and fibrotic cells, and increased senescence in vitro. Upon in vivo transplantation into mice, TBD-BMSCs failed to form bone or support hematopoiesis, unlike normal BMSCs. TERC reduction (a TBD-associated gene) in normal BMSCs by siTERC-RNA recapitulated the TBD-BMSC phenotype by reducing proliferation and secondary colony forming efficiency, and by accelerating senescence in vitro. Microarray profiles of control and siTERC-BMSCs showed decreased hematopoietic factors at the mRNA level, and decreased secretion of factors at the protein level. These findings are consistent with defects in SSCs/BMSCs contributing to bone marrow failure in TBD.
2014-12-09 | GSE64023 | GEO
Project description:The natural history of multiple myeloma is characterized by its localization to the bone marrow and its interaction with bone marrow stromal cells. The bone marrow stromal cells provide growth and survival signals, thereby promoting the development of drug resistance. Here, we show that the interaction between bone marrow stromal cells and myeloma cells (using human cell lines) induces chromatin remodeling of cis-regulatory elements and is associated with changes in the expression of genes involved in the cell migration and cytokine signaling. The expression of genes involved in these stromal interactions are observed in extramedullary disease in patients with myeloma and provides the rationale for survival of myeloma cells outside of the bone marrow microenvironment. Expression of these stromal interaction genes is also observed in a subset of patients with newly diagnosed myeloma and are akin to the transcriptional program of extramedullary disease. The presence of such adverse stromal interactions in newly diagnosed myeloma is associated with accelerated disease dissemination, predicts the early development of therapeutic resistance, and is of independent prognostic significance. These stromal cell induced transcriptomic and epigenomic changes both predict long-term outcomes and identify therapeutic targets in the tumor microenvironment for the development of novel therapeutic approaches.
2024-04-04 | GSE263178 | GEO
Project description:The bone marrow is continuously occupied by high numbers of neutrophils, and a tumor-supportive bias of these cells could significantly impact bone marrow-confined malignancies. In multiple myeloma, the bone marrow is characterized by inflammatory stromal cells with the potential to influence neutrophils. Here, we investigated myeloma-associated alterations in marrow neutrophils and the impact of stromal inflammation on neutrophil function. Mature neutrophils in myeloma marrow are activated and tumor-supportive, transcribing increased levels of pro-inflammatory cytokines, including IL-1β, and myeloma cell survival factors, such as the BCMA-ligand BAFF. Neutrophils were re-activated after first-line treatment, while this regimen reduced, but did not normalize, stromal inflammation. Interactions with inflammatory stroma induced neutrophil activation, including BAFF secretion, in a STAT3-dependent manner and once activated, neutrophils gained the ability to reciprocally induce stromal activation. Combined, our data define the presence of a neutrophil-stromal cell feed-forward loop driving tumor-supportive inflammation that could impact disease recurrence.
| EGAS00001007038 | EGA