Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

RNA-seq analysis of bone marrow stromal and hematopoietic TNCs

ABSTRACT: Bone marrow stromal cells are commonly defined by CD45–Ter119–CD31– (Triple-negative cells or TNCs). In this study, we show that most TNCs are not labeled by mesenchymal cell genetic labeling models but are derived from hematopoietic stem and progenitor cells. RNA-Seq analysis of TNCs reveals erythroid and lymphoid progenitor signatures among CD51– TNCs which was confirmed by in vitro culture studies with primary bone marrow stromal cells and by in vivo transplantation experiments. We also show that CD44+CD51– TNCs expands during phenylhydrazine-induced hemolytic anemia and in a mouse model of sickle cell disease. These results uncover new classes of stromal-associated hematopoietic progenitors.

ORGANISM(S): Mus musculus

PROVIDER: GSE107775 | GEO | 2020/12/05

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

Hematopoietic origin of most CD45– bone marrow cells

Project description:The non-hematopoietic cell fraction of the bone marrow (BM) is classically identified as CD45– Ter119– CD31– (herein referred to as triple-negative cells or TNCs). Although TNCs are believed to contain heterogeneous stromal cell populations, they remain poorly defined. Here we show, unexpectedly, that the vast majority of TNCs (~85%) have a hematopoietic rather than mesenchymal origin. Single cell RNA-sequencing reveals erythroid and lymphoid progenitor signatures among CD51– TNCs. When cultured with BM-derived stromal cells, Ly6D+ CD44+ CD51–TNCs give rise to B-lymphoid cells, whereas Ly6D–CD44+ CD51–TNCs generate erythroid cells. In addition, CD44+ CD51– TNCs contribute to repopulate B-lymphoid and erythroid cells after transplantation in mice. The CD44+ CD51– TNC population also expands during phenylhydrazine-induced acute hemolysis or in a model of sickle cell anemia. These findings thus uncover physiologically relevant, yet unappreciated, classes of stromal-associated CD45– hematopoietic progenitors.

2021-04-23 | GSE113544 | GEO

Bulk RNA sequencing of endothelial-derived and non-endothelial-derived BMSCs and OLCs of VE-Cadherin-Cre;LoxP-tdTomato mice

Project description:We performed lineage tracing experiments using VE-Cadherin-Cre;LoxP-tdTomato mice. In these mice, endothelial cells (ECs) and their progeny are permanently marked by tdTomato fluorescence. We found that a substantial subset of stromal cells is derived from ECs, as indicated by their tdTomato expression. These findings support the notion that endothelial to mesenchymal transition (EndoMT) contributes to hematopoietic bone marrow niche formation in mice. Here we sought to determine the transcriptomic differences between endothelial-derived (tdTomato-positive) and non-endothelial-derived (tdTomato-negative) bone marrow stromal cells (BMSCs) and osteo/chondrolineage progenitor cells (OLCs). Murine niche populations were obtained from collagenased bone fraction of VE-Cadherin-Cre;LoxP-tdTomato mice at 3 weeks (n=2) or 11 weeks (n=2) of age. BMSCs (CD45-TER119-CD31-CD144-SCA-1+ CD51+ cells) and OLCs (CD45-TER119-CD31-CD144-Sca1-CD51+ cells) were FACS-purified and sequenced.

2021-01-25 | E-MTAB-10020 | biostudies-arrayexpress

RNAseq analysis of bone marrow mesenchymal stem cells

Project description:The phenotype of bone marrow mesenchymal stem cells in the murine Townes model of sickle cell disease is not well characterized. We analyzed differences in the gene signature between SA and SS MSCs. MSCs were defined by CD45-Ter119-CD31-CD51+CD140a+ surface expression. We identified significant differences in SS MSC gene profile and stem cell functionality compared to SA control MSCs.

2021-12-23 | GSE159373 | GEO

Harnessing matrix stiffness to engineer a bone marrow niche for hematopoietic stem cell rejuvenation

Project description:RNA and ATAC sequencing data of primary sorting CD45-Ter119-CD31-Scf; GFP+Cxcl12; DsRed+ bone marrow stromal cells ,2D cultured bone marrow stromal cells and 3D cultured bone marrow stromal cells. RNA sequencing data of sorted primary and 3D cocultured Lin-Sca1+C-kit+CD150+CD48+ hematopoietic stem cells from 8-12 weeks and 12-13 months old mice. RNA and ATAC sequencing data of primary sorting CD45-Ter119-CD31-Pdgfra+td-Tomato+ bone marrow stromal cells from young (8 wks), middle aged (12 months) and aged (22-24 months) Lepr-Cre;td-Tomato mice.

2023-04-06 | GSE180866 | GEO

Stromal inflammation is a targetable driver of blood aging [droplet-based scRNAseq - Batch 2]

Project description:To investigate the role of IL1 signaling in hematopoietic aging, we performed droplet-based scRNAseq (10X Genomics) of hematopoietic stem and progenitor cells (LK/LSK) and unfractionated endosteal and central marrow stromal cells (Ter119-/CD45-) from young wild type and young and old wild type and IL1R1-/- C57BL/6 mice.

2022-11-02 | GSE189217 | GEO

Transcriptome analysis of synovial osteoprogenitor populations in mice with antigen-induced arthritis and non-immunized mice

Project description:The aim of this experiment was to analyze differences in gene expression between potential osteoprogenitor populations in synovial compartment of non-immunized mice and mice with antigen-induced arthritis (AIA). We analyzed transcriptome of TER119–CD31–CD45–CD51+CD200+CD105– cells from nonimmunized mice, TER119–CD31–CD45–CD51+CD200+CD105– cells from mice with arthritis, and TER119–CD31–CD45–CD51+CD200–CD105+ from mice with arthritis. Comparison between nonimmunized and arthritic mice served to determine changes in TER119–CD31–CD45–CD51+CD200+CD105–population induced by arthritis. Comparison of TER119–CD31–CD45–CD51+CD200+CD105– and TER119–CD31–CD45–CD51+CD200–CD105+ from mice with arthritis aimed to define transcriptomic differences between those two populations.

2020-05-05 | GSE148130 | GEO

Stromal inflammation is a targetable driver of hematopoietic aging [droplet-based scRNAseq]

Project description:To investigate global changes in the structure of the bone marrow niche with age, we performed droplet-based scRNAseq (10X Genomics) of unfractionated endosteal and central marrow stromal cells (Ter119-/CD45-). 8,735 cells passed QC, and hematopoietic clusters of cells were excluded based on marker gene expression, leaving 2359 cells distributed across 9 distinct clusters for final presentation.

2022-11-02 | GSE168586 | GEO

scRNA-seq of Chrna7+ bone marrow stromal cells in Chat-fl/fl and Cd19-Cre Chat-fl/fl mice

Project description:Examination of gene expression in FACS-purified Ter119- CD45- Chrna7+ bone marrow stromal cells as a function of B cell-derived acetylcholine

2022-03-09 | GSE157885 | GEO

Heme exposure shifts shifts myeloid differentiation in bone marrow derived mixed cell cultures.

Project description:Heme is an erythrocyte-derived toxin that drives disease progression in hemolytic anemias. During hemolysis, specialized bone marrow-derived macrophages with a high heme-metabolism capacity orchestrate disease adaptation by removing damaged erythrocytes and heme-protein complexes from the blood and supporting iron recycling for erythropoiesis. Here, we performed single-cell RNA sequencing with RNA velocity analysis of GM-CSF-supplemented mouse bone marrow cultures to assess myeloid differentiation under heme stress. We found that heme-activated NRF2 signaling shifted the differentiation trajectories of cells towards antioxidant, iron-recycling macrophages at the expense of dendritic cells, as these cells were selectively deficient in heme-exposed bone marrow cultures. Heme eliminated the capacity of GM-CSF-supplemented bone marrow cultures to activate antigen-specific T cells. The generation of functionally competent dendritic cells was restored by NRF2 loss. The heme-induced phenotype was reproduced in hemolytic mice with sickle cell disease and spherocytosis and associated with reduced dendritic cell functions in the spleen. Our data provide a novel mechanistic underpinning how hemolytic stress may provoke hyposplenism-related secondary immunodeficiency, which is a critical determinant of mortality in patients with genetic hemolytic anemias.

2022-01-25 | GSE179362 | GEO

Heme signaling shifts myeloid differentiation in GM-CSF BM cell cultures

2022-01-25 | GSE179360 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data