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

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

ORGANISM(S): Mus musculus

PROVIDER: GSE225442 | GEO | 2023/02/17

REPOSITORIES: GEO

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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 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

Next Generation Sequencing of long-term hematopoietic cells (LT-HSCs) with or without mutations in JAK2 and Ezh2

Project description:Comparison of mRNA expression profiles of LT-HSCs with or without mutations in JAK2 and Ezh2 by RNA sequencing. LT-HSC mRNA was extracted from six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) 10 weeks after tamoxifen injection. Our study represents the first detailed analysis of mRNA expression profile of LT-HSC with or without mutations in JAK2 and Ezh2 , with biologic replicates, generated by RNA-seq technology. Our results revealed that mRNA expression profile of LT-HSC with different genotype showed specific gene expression patterns, which allows to do biological comprehensive and quantitative analysis for hematopoiesis. LT-HSCs mRNA profiles six different transgenic mice (SclCre, SclCre;Ezh2+/-, SclCre;Ezh2-/-, SclCre; JAK2V617F, SclCre; JAK2V617F;Ezh2+/-, SclCre; JAK2V617F;Ezh2-/-) were generated by deep sequencing.

2016-06-24 | E-GEOD-82073 | biostudies-arrayexpress

Expression in LT-HSC after in vitro culture in mSCF, mTpo, mFlt3L, hIGFBP2 and Angptl5.

Project description:Mouse LT-HSC were sorted and cultured in mScf, mTpo, mFlt3L, hIGFBP2 and Angptl5 for 2 days. These expression values were related to insertions of gamma-retroviral, lentiviral or alpharetroviral vectors carrying GFP which were retrieved after serial murine BM transplantation. The relation between gene expression in the cells responsible for long-term hematopoiesis and location of vector integration was investigated. Biological duplicate measurements of murine sorted and cultured LT-HSC (LSK, CD34-, CD135-)

2011-12-28 | E-GEOD-34731 | biostudies-arrayexpress

Expression data from TFIIA-non-cleavable mouse fetal liver hematopoietic stem cells

Project description:During embryogenesis, development of hematopoietic stem cells (HSC) occurs in the fetal liver and involves coordinate programs of transcription. Taspase1, a highly conserved threonine protease, directly cleaves and regulates the TFIIA families of transcription factors. We discovered that loss of Taspase1 (Tasp1-/-) or non-cleavage of TFIIAa-b (TFIIAa-b nc/nc) leads to a severe fetal liver developmental retardation that is associated with impaired HSC self-renewal and loss of HSC quiescence. We used microarray to elucidate the mechanism(s) by which TFIIA regulates fetal liver hematopoiesis, and expression of targets of HoxA9 was found to be altered by gene set enrichment analyses. Embryonic day 14.5 fetal liver HSCs (defined as Lineage-Sca-1+c-Kit+CD150+cells) of wild-type (n = 4) and TFIIAa-b nc/nc (n = 3) were analyzed.

2014-05-28 | E-GEOD-47422 | biostudies-arrayexpress

Expression data from TFIIA-non-cleavable mouse fetal liver hematopoietic stem cells

Project description:During embryogenesis, development of hematopoietic stem cells (HSC) occurs in the fetal liver and involves coordinate programs of transcription. Taspase1, a highly conserved threonine protease, directly cleaves and regulates the TFIIA families of transcription factors. We discovered that loss of Taspase1 (Tasp1-/-) or non-cleavage of TFIIAα−β (TFIIAα-βnc/nc) leads to a severe fetal liver developmental retardation that is associated with impaired HSC self-renewal and loss of HSC quiescence. We used microarray to elucidate the mechanism(s) by which TFIIA regulates fetal liver hematopoiesis, and expression of targets of HoxA9 was found to be altered by gene set enrichment analyses.

2014-05-28 | GSE47422 | GEO

Next Generation Sequencing of long-term hematopoietic cells (LT-HSCs) with or without mutations in JAK2 and Ezh2

2016-06-24 | GSE82073 | GEO

HSCs contribute actively to native multilineage hematopoiesis but with reduced differentiation capacity upon aging

Project description:A hallmark of adult hematopoiesis is the continuous replacement of blood cells with limited lifespans. While active hematopoietic stem cell (HSC) contribution to multilineage hematopoiesis is the foundation of clinical HSC transplantation, recent reports have questioned the physiological contribution of HSCs to normal/steady-state adult hematopoiesis. Here, we use inducible lineage tracing from genetically marked adult HSCs and reveal robust HSC-derived multilineage hematopoiesis. This commences via defined progenitor cells, but varies substantially in between different hematopoietic lineages. By contrast, adult HSC contribution to hematopoietic cells with proposed fetal origins is neglible. Finally, we establish that the HSC contribution to multilineage hematopoiesis declines with increasing age. Therefore, while HSCs are active contributors to native adult hematopoiesis, it appears that the numerical increase of HSCs is a physiologically relevant compensatory mechanism to account for their reduced differentiation capacity with age

2018-12-18 | GSE122473 | 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

Endomucin marks quiescent long-term multi-lineage repopulating hematopoietic stem cells and is essential for their transendothelial migration [RNA-seq: wildtype_EMCN]

Project description:Endomucin (EMCN) currently represents the only hematopoietic stem cell (HSC) marker expressed by both murine and human HSCs. Here, we report that EMCN+ long-term repopulating HSCs (LT-HSCs; CD150+CD48−LSK) have a higher long-term multi-lineage repopulating capacity compared to EMCN− LT-HSCs. Cell cycle analyses and transcriptional profiling demonstrated that EMCN+ LT-HSCs were more quiescent compared to EMCN− LT-HSCs. Emcn−/− and Emcn+/+ mice displayed comparable steady-state hematopoiesis, as well as frequencies, transcriptional programs, and long-term multi-lineage repopulating capacity of their LT-HSCs. Complementary functional analyses further revealed increased cell cycle entry upon treatment with 5-fluorouracil and reduced granulocyte colony-stimulating factor (GCSF) mobilization of Emcn−/− LT-HSCs, demonstrating that EMCN expression by LT-HSCs associates with quiescence in response to hematopoietic stress and is indispensable for effective LT-HSC mobilization. Transplantation of wild-type bone marrow cells into Emcn−/− or Emcn+/+ recipients demonstrated that EMCN is essential for endothelial cell-dependent maintenance/self-renewal of the LT-HSC pool and sustained blood cell production post-transplant.

2024-07-23 | GSE222941 | GEO

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