Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [scRNA-seq]

ABSTRACT: We investigate the heterogeneity of macrophage populations in the fetal liver to define their specific roles during hematopoiesis.

ORGANISM(S): Mus musculus

PROVIDER: GSE225443 | GEO | 2023/02/17

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [bulkRNA-seq]

Project description:Investigating the effect of macrophages on the function of LT-HSC and hematopoiesis during embryogenesis in the fetal liver

2023-02-17 | GSE225442 | GEO

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesis.

Project description:During embryogenesis, the fetal liver becomes the main hematopoietic organ, where stem and progenitor cells as well as immature and mature immune cells form an intricate cellular network. Hematopoietic stem cells (HSCs) reside in a specialized niche, which is essential for their proliferation and differentiation. However, the cellular and molecular determinants contributing to this fetal HSC niche remain largely unknown. Macrophages are the first differentiated hematopoietic cells found in the developing liver, where they are important for fetal erythropoiesis by promoting erythrocyte maturation and phagocytosing expelled nuclei. Yet, whether macrophages play a role in fetal hematopoiesis beyond serving as a niche for maturing erythroblasts remains elusive. Here, we investigate the heterogeneity of macrophage populations in the murine fetal liver to define their specific roles during hematopoiesis. Using a single-cell omics approach combined with spatial proteomics and genetic fate-mapping models, we found that fetal liver macrophages cluster into distinct yolk sac-derived subpopulations and that long-term HSCs are interacting preferentially with one of the macrophage subpopulations. Fetal livers lacking macrophages show a delay in erythropoiesis and have an increased number of granulocytes, which can be attributed to transcriptional reprogramming and altered differentiation potential of long-term HSCs. Together, our data provide a detailed map of fetal liver macrophage subpopulations and implicate macrophages as part of the fetal HSC niche.

| S-EPMC11006421 | biostudies-literature

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [scRNA-seq]

Project description:Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [scRNA-seq]

| PRJNA935719 | ENA

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-02-17 | GSE225444 | GEO

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi

Project description:Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi

| PRJNA935711 | ENA

Spatial transcriptome profiling by MERFISH reveals fetal liver hematopoietic stem cell niche architecture [scRNA-seq]

Project description:The hematopoietic stem cell (HSC) niche has been extensively studied in bone marrow, yet a more systematic investigation into the microenvironment regulation of hematopoiesis in fetal liver is necessary. Here we investigate the spatial organization and transcriptional profile of individual cells in both wild type and Tet2-/- fetal livers, by multiplexed error robust fluorescence in situ hybridization (MERFISH). We find that specific pairs of fetal liver cell types are preferentially positioned next to each other. Ligand-receptor singling molecule pairs such as Kitl and Kit are enriched in neighboring cell types. The majority of HSCs are directly in contact with endothelial cells (ECs) in both wild type and Tet2-/- fetal livers. Loss of Tet2 increases the number of HSCs, and upregulates Wnt and Notch signaling genes in the HSC niche. Two subtypes of ECs – arterial ECs and sinusoidal ECs – and other cell types contribute distinct signaling molecules to the HSC niche. Collectively, this study provides a comprehensive picture and bioinformatic foundation for HSC spatial regulation in fetal liver.

2021-04-16 | GSE172127 | GEO

Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [bulkRNA-seq]

Project description:Fetal liver macrophages contribute to the hematopoietic stem cell niche by controlling granulopoiesi [bulkRNA-seq]

| PRJNA935721 | ENA

Maternal Immune Activation perturbs fetal hematopoietic development and causes persistent changes to postnatal immunity [scRNA-Seq']

Project description:Adult hematopoietic stem cells (HSCs) respond directly to inflammation and infection, resulting in both acute and persistent changes in quiescence, mobilization, and differentiation. Here we show that fetal HSCs respond to maternal inflammation in utero, and the fetal response drives long-term changes to postnatal hematopoiesis and immunity. Heterogeneous fetal hematopoietic stem and progenitor cells (HSPCs) show divergent responses to maternal immune activation (MIA), including changes in quiescence, expansion, and immune cell output. Single cell transcriptomic analysis of fetal HSPCs reveals specific upregulation of inflammation-responsive genes in discrete populations, in response to upregulated IFNα and IL-1α in the fetal liver cytokine milieu. Postnatally, MIA caused the inappropriate expansion and persistence of transient progenitors, concomitant with increased cellularity and hyper-responsiveness of fetal-derived immune cells. Our investigation demonstrates how inflammation in utero can direct the trajectory of hematopoiesis and immunity by reshaping fetal HSC establishment.

2023-01-27 | GSE161926 | GEO

C-Myb+ erythro-myeloid progenitor-derived fetal monocytes give rise to adult tissue-resident macrophages

Project description:Although classified as hematopoietic cells, tissue-resident macrophages are selfrenewing and maintained independently of adult hematopoiesis. While most macrophages originate from embryonic precursors that seed tissues prior to birth, their exact origin is unknown. Using an in utero macrophage depletion strategy and fatemapping of yolk sac (YS) and fetal liver (FL) hematopoiesis, we found that YS macrophages are the main precursors of microglia, while most other macrophages derive from fetal monocytes. Both YS macrophages and fetal monocytes arise from erythro-myeloid progenitors (EMP) generated in the YS. In the YS, EMP gave rise to macrophages without monocytic intermediates, while EMP seeding the FL upon the establishment of blood circulation acquired c-Myb expression and gave rise to fetal monocytes that then seed embryonic tissues to differentiate into macrophages. Thus, adult tissue-resident macrophages established from HSC-independent embryonic precursors arise from two different developmental programs. 12 samples of progenitors, monocytes or macrophages are analyzed from 2 to 4 replicate. Each replicate derived from at least 5 embryos or adult mice

2015-04-23 | E-GEOD-66970 | biostudies-arrayexpress

C-Myb+ erythro-myeloid progenitor-derived fetal monocytes give rise to adult tissue-resident macrophages

2015-04-23 | GSE66970 | GEO