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

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

PROVIDER: PRJNA935719 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23498437.fastq.gz	Fastqsanger.gz
	SRR23498438.fastq.gz	Fastqsanger.gz
	SRR23498439.fastq.gz	Fastqsanger.gz
	SRR23498440.fastq.gz	Fastqsanger.gz
	SRR23498441.fastq.gz	Fastqsanger.gz

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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

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

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

2023-02-17 | GSE225443 | GEO

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

Identification of a portal vessel-associated fetal liver hematopoietic stem cell niche

Project description:Whereas the cellular basis of the hematopoietic stem cell (HSC) niche in the bone marrow has been characterized, the nature of the fetal liver (FL) niche is not yet elucidated. We show that Nestin+NG2+ pericytes associate with portal vessels, forming a niche promoting HSC expansion. Nestin+NG2+ cells and HSCs scale during development with the fractal branching patterns of portal vessels, tributaries of the umbilical vein. After closure of the umbilical inlet at birth, portal vessels undergo a transition from Neuropilin-1+Ephrin-B2+ artery to EphB4+ vein phenotype, associated with a loss of peri-portal Nestin+NG2+ cells and emigration of HSCs away from portal vessels. These data support a model in which HSCs are titrated against a peri-portal vascular niche with a fractal-like organization enabled by placental circulation. Characterization of the transcriptome of fetal liver and adult bone marrow niche using RNA-seq

2015-12-03 | E-GEOD-72341 | biostudies-arrayexpress

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

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

2021-04-16 | GSE172128 | GEO

Identification of a portal vessel-associated fetal liver hematopoietic stem cell niche

2015-12-03 | GSE72341 | GEO

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