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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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Single-cell RNAseq of human bone marrow cells (Drop-seq)

ABSTRACT: Gene expression profiles of individual bone marrow cells were acquired by Drop-Seq. Total bone marrow (TBM) and weakly lineage depleted bone marrow (DBM; CD235a and/or Cd45 negative) and stromal cells (STRO-1 positive or collagenase IV released) were analysed.

INSTRUMENT(S): NextSeq 500

ORGANISM(S): Homo sapiens

SUBMITTER: Ben MacArthur

PROVIDER: E-MTAB-8629 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Transfer learning efficiently maps bone marrow cell types from mouse to human using single-cell RNA sequencing.

Stumpf Patrick S PS Du Xin X Imanishi Haruka H Kunisaki Yuya Y Semba Yuichiro Y Noble Timothy T Smith Rosanna C G RCG Rose-Zerili Matthew M West Jonathan J JJ Oreffo Richard O C ROC Farrahi Katayoun K Niranjan Mahesan M Akashi Koichi K Arai Fumio F MacArthur Ben D BD

Communications biology 20201204 1

Biomedical research often involves conducting experiments on model organisms in the anticipation that the biology learnt will transfer to humans. Previous comparative studies of mouse and human tissues were limited by the use of bulk-cell material. Here we show that transfer learning-the branch of machine learning that concerns passing information from one domain to another-can be used to efficiently map bone marrow biology between species, using data obtained from single-cell RNA sequencing. We ...[more]

PMID: 33277618

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Single-cell RNAseq of human bone marrow cells enriched for stromal and endothelial markers

Project description:Gene expression profiles of individual bone marrow cells were acquired by Drop-Seq. Subsets of bone marrow cells were isolated using magnetic cell sorting to enrich for putative skeletal stem cells.

2021-06-30 | E-MTAB-9662 | biostudies-arrayexpress

Single-cell RNAseq of mouse bone marrow cells (Drop-seq)

Project description:Gene expression profiles of individual bone marrow cells were acquired by Drop-Seq. Total bone marrow (TBM) and weakly depleted bone marrow (DBM; Ter119/Cd45 negative cells) were analysed.

2020-11-27 | E-MTAB-8630 | biostudies-arrayexpress

Single-cell RNAseq of human bone marrow cells enriched using RNA probes

Project description:Gene expression profiles of individual bone marrow cells were acquired by Drop-Seq. Subsets of bone marrow cells were isolated using fluorescence-assisted cell sorting to enrich for putative skeletal stem cells.

2022-05-31 | E-MTAB-9664 | biostudies-arrayexpress

Mito-protective autophagy is impaired in erythroid cells of aged mtDNA-mutator mice

Project description:Somatic mitochondrial DNA (mtDNA) mutations contribute to the pathogenesis of age-related disorders, including myelodysplastic syndromes (MDS). The accumulation of mitochondria harboring mtDNA mutations in patients with these disorders suggests a failure of normal mitochondrial quality-control systems. The mtDNA-mutator mice acquire somatic mtDNA mutations via a targeted defect in the proofreading function of the mtDNA polymerase, PolgA, and develop macrocyticanemia similar to that of patients with MDS. We observed an unexpected defect in clearance of dysfunctional mitochondria at specific stages during erythroid maturation in hematopoietic cells from aged mtDNA-mutator mice. Mechanistically, aberrant activation of mechanistic target of rapamycin signaling and phosphorylation of uncoordinated 51-like kinase (ULK) 1 in mtDNA-mutator mice resulted in proteasome mediated degradation of ULK1 and inhibition of autophagy in erythroid cells. To directly evaluate the consequence of inhibiting autophagy on mitochondrial function in erythroid cells harboring mtDNA mutations in vivo, we deleted Atg7 from erythroid progenitors of wildtype and mtDNA-mutator mice. Genetic disruption of autophagy did not cause anemia in wild-type mice but accelerated the decline in mitochondrial respiration and development of macrocytic anemia in mtDNA-mutator mice. These findings highlight a pathological feedback loop that explains how dysfunctional mitochondria can escape autophagy-mediated degradation and propagate in cells predisposed to somatic mtDNA mutations, leading to disease. We used microarrays to identify expression profiles and pathways that are differentially activated or suppressed in Ter119+ bone marrow cells isolated from phlebotomized wildtype or Polg mutant mice

2015-04-21 | E-GEOD-57761 | biostudies-arrayexpress

Cellular adhesion promotes prostate cancer cells escape from dormancy

Project description:Dissemination of prostate cancer (PCa) cells to the bone marrow is an early event in the disease process. In some patients, following initial treatment, disseminated tumor cells (DTC) proliferate to form active metastases after a prolonged period of undetectable disease known as tumor dormancy. Identifying mechanisms of PCa dormancy and reactivation remain a challenge due to the lack of in vitro models. Here, we characterized in vitro PCa dormancy-reactivation by inducing three apparently dormant patient-derived xenograft (PDX) lines to proliferate through tumor cell contact with each other and with bone marrow stroma. Proliferating PCa cells demonstrated tumor cell-cell contact and integrin clustering on immunofluorescence. Global gene expression analyses on proliferating cells cultured on bone marrow stroma revealed a downregulation of TGFB2 in all of the three proliferating PCa PDX lines when compared to their non-proliferating counterparts. Furthermore, constitutive activation of myosin light chain kinase (MLCK), a downstream effector of integrin-beta1 and TGF-beta2, in non-proliferating cells resumed cell proliferation. This cell proliferation was associated with an upregulation of CDK6 and a downregulation of E2F4. Taken together, our data provide evidence to support cellular adhesion and downregulation of TGFB2 as a potential mechanism by which PCa cells escape from dormancy. Targeting TGF-beta 2-associated mechanism could provide novel opportunities to prevent lethal PCa metastasis. Custom Agilent-016162 44K whole human genome expression oligonucleotide microarrays were used to profile dormant and proliferating cells isolated from three separate LuCaP xenograft lines grown in co-culture with bone marrow stromal cells isolated from a patient with PCa bone metastases. RNA from 10 cells was amplified prior to hybridization against a common reference pool of prostate tumor cell lines.

2015-10-26 | E-GEOD-64262 | biostudies-arrayexpress

Hematopoietic Transcriptional Comparison of HSC from B10.BR/JRep and B10.BR/J (drifted) mice

Project description:Divergence has occured between the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains, resulting in altered antigenic recognition and differential bone marrow engraftment capability. The microarray data demonstrate that the transcriptional profile of genes associated with hematopoiesis differs between lineage negative (as a marker for hematopoietic stem cells) bone marrow cells isolated from the B10.BR-H2k H2-T18a/SgSnJJrep and B10.BR-H2k H2-T18a/SgSnJ (drifted) mouse strains. Bone marrow cells from ten male mice of each strain, aged 10-12 weeks, were harvested. One pooled sample was analyzed for each strain.

2009-09-15 | E-GEOD-17471 | biostudies-arrayexpress

scRNAseq for bone marrow cells from Cebpαcre/+ R26EYFP/+ SbdsF/F (neutropenia) mice vs Cebpαcre/+ R26EYFP/+ Sbds+/+ (Ctrl) mice

Project description:To delineate the potential molecular mechanisms underlying the communication between neutrophils and NK cells, we performed scRNAseq of the neutropenic bone marrow (12 months after transplantation of Cebpacre/+ Sbds +/+ or F/F cells). To this end, bone marrow cells were subsorted into HSC+MPP (LKS CD48-), HPC1 (LKS CD48+CD150-), B and T cells (B220+, CD3+), NK cells (NK1.1+ NKp46+) and a myeloid ‘rest’ fraction (B220-,CD3-,NKp46- and NK1.1-) and sorted fractions pooled together to obtain robust representation of all bone marrow cell types in the scRNAseq data

2022-12-31 | E-MTAB-12428 | biostudies-arrayexpress

Combined miRNA and mRNA analysis of CD133(+) and CD34(+) cells

Project description:Microarray and miRNA analysis of CD133(+), CD34(+)CD133(-) and CD133(-)CD34(-) cells The goal of the experiment was the comparison of expression levels of mRNA and miRNA in CD133(+) and CD34(+)CD133(-) cells The RNA of CD133(+), CD34(+)CD133(-) and CD133(-)CD34(-) bone marrow cells was amplified by using the µMACSTM SuperAmpTM Kit (Miltenyi Biotec).

2011-03-14 | E-GEOD-22460 | biostudies-arrayexpress

Paired scRNAseq of the and non-hematopoietic and the immune microenvironment of aspirates from newly diagnosed Multiple Myeloma patients versus non-cancer controls

Project description:By generating a paired single cell RNA-sequencing database of the tumor niche from 10 newly diagnosed MM patients, we created a unique dataset allowing the in-depth analyses of stromal-immune interactions within the tumor microenvironment. Using this database, we identified the presence of inflammatory stromal fibroblasts in the bone marrow of Myeloma patients.The stromal inflammation was associated with NF-κB signaling, and sources of IL-1β or TNFα were specific immune subsets previously shown to be altered in MM, suggesting the presence of an immune cell-mediated feed-forward loop of bone marrow inflammation in MM. By tracking inflammatory signatures over time in individual patients undergoing first-line treatment using bulk RNA sequencing, we show that bone marrow inflammation is not reverted by successful anti-tumor therapy (see related accession number), suggesting a role for stromal fibroblasts and bone marrow inflammation in disease persistence or relapse.

2020-09-30 | E-MTAB-9139 | biostudies-arrayexpress

RNA sequencing of the non-hematopoietic microenvironment of aspirates from Multiple Myeloma patients at diagnosis and after treatment versus non-cancer controls

Project description:By generating a paired single cell RNA-sequencing database of the tumor niche from 10 newly diagnosed MM patients, we created a unique dataset allowing the in-depth analyses of stromal-immune interactions within the tumor microenvironment (see related accession number). Using this database, we identified the presence of inflammatory stromal fibroblasts in the bone marrow of Myeloma patients.The stromal inflammation was associated with NF-κB signaling, and sources of IL-1β or TNFα were specific immune subsets previously shown to be altered in MM, suggesting the presence of an immune cell-mediated feed-forward loop of bone marrow inflammation in MM. By tracking inflammatory signatures over time in individual patients undergoing first-line treatment using bulk RNA sequencing, we show that bone marrow inflammation is not reverted by successful anti-tumor therapy (this dataset), suggesting a role for stromal fibroblasts and bone marrow inflammation in disease persistence or relapse. Raw sequencing data files will be deposited to EGA.

2021-02-01 | E-MTAB-9285 | biostudies-arrayexpress

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