Homo sapiens
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA236141 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Expression data of human fetal liver hematopoietic stem and progenitors cells [Set 1]
| PRJNA236142 | ENA
Project description:Proteomics reveals dynamic metabolic changes of human hematopoietic stem progenitor cells from fetal liver to adult stages
2024-05-10 | PXD052196 |
Project description:Human pluripotent stem cells were differentiated into hematopoietic progenitors, which were then re-specified using defined transcription factors to resemble hematopoietic stem cells (HSC) We used microarrays to establish the similarity between converted cells and purified human HSCs. The samples analyzed were: starting embryoid body progenitors, transcription factor-converted cells, and primary HSCs and progenitors from fetal liver and cord blood. All samples were flow sorted for CD34+ and CD38- to compare across a similar population of primitive cells.
2013-11-01 | E-GEOD-49938 | biostudies-arrayexpress
Project description:Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal. We used microarrays to identify genes enriched in the GPI-80+ hematopoietic stem and progenitor population in fetal liver. RNA was extracted from enriched fetal liver hematopoietic stem and progenitor cells, and downstream progenitors, for comparison based on Affymetrix arrays.
2015-01-23 | E-GEOD-54315 | biostudies-arrayexpress
Project description:Advances in pluripotent stem cell and reprogramming technologies have given hope of generating hematopoietic stem cells (HSC) in culture. To succeed, greater understanding of the self-renewing HSC during human development is required. We discovered that glycophosphatidylinositol-anchored surface protein GPI-80 (Vanin 2) defines a distinct subpopulation of human fetal hematopoietic stem/progenitor cells (HSPC) with self-renewal ability. CD34+CD90+CD38-GPI-80+ HSPC were the sole population that maintained proliferative potential and undifferentiated state in bone marrow stroma co-culture, and engrafted in immunodeficient mice. GPI-80 expression also enabled tracking of HSC migration between human fetal hematopoietic niches. The most highly enriched surface protein in GPI-80+ HSPC as compared to their progeny was Integrin alpha-M (ITGAM), which in leukocytes cooperates with GPI-80 to support migration. Knockdown of either GPI-80 or ITGAM was sufficient to perturb undifferentiated HSPC in stroma co-culture. These findings indicate that human fetal HSC utilize common mechanisms with leukocytes for cell-cell interactions governing HSC self-renewal. We used microarrays to identify genes enriched in the CD90+ hematopoietic stem and progenitor population in fetal liver. RNA was extracted from enriched fetal liver hematopoietic stem and progenitor cells, and downstream progenitors, for comparison based on Affymetrix arrays.
2015-01-23 | E-GEOD-54314 | biostudies-arrayexpress
Project description:Development of red blood cells from progenitors requires profound reshaping of both gene expression and metabolism. How these processes are coupled is unclear. Nprl3, an inhibitor of mTORC1, has remained in synteny with the -globin genes for >500 million years, and harbours most of the -globin enhancers. However, whether Nprl3 itself serves an erythroid role is unknown. While hematopoietic progenitors rely on tonic expression of baseline Nprl3, erythroblasts experience ‘boosted’ Nprl3 expression. Using Nprl3-deficient fetal liver and adult competitive bone marrow - fetal liver chimaeras, we show that NprI3 is required for sufficient erythropoiesis. Loss of Nprl3 elevates mTORC1 signalling, suppresses autophagy and disrupts erythroblast glycolysis. Human NPRL3-knockout erythroid progenitors produce fewer enucleated cells and demonstrate dysregulated mTORC1 signalling in response to nutrient availability and erythropoietin. Thus, Nprl3 is a key regulator of erythroid metabolism. Finally, we show that the alpha-globin enhancers upregulate erythoid NprI3 expression, and that this activity supports optimal erythropoiesis.
2025-02-12 | PXD060557 | Pride
Project description:Reprogramming of Human Fibroblasts into Hematopoietic Progenitors by Fusion With Human Fetal Liver CD34+ Cells (GenomeWideSNP_6)
| PRJNA133343 | ENA
Project description:The emergence of the hematopoietic system occurs in temporal waves across different tissues during mouse development. During these waves, the endothelial niche serves as a source of hematopoietic cells and provides molecular cues that potentially shape the tissue-specific lineage output. Although the endothelial-to-hematopoietic transition in the aorta-gonad-mesonephros is well understood, a systematic analysis of hematopoietic progenitors and their endothelial niche across fetal tissues is lacking. Here, we leverage single-cell RNA-sequencing of micro-dissected fetal tissues during their peak of hematopoietic activity to systematically compare hematopoietic progenitors and the endothelial niche. We predict stage-specific interactions accompanying the transition of yolk sac endothelium to primitive and definitive hematopoietic fates and reveal distinct roles for fetal liver vascular niches. Furthermore, we provide in vitro evidence that lipid signaling by sphingosine-1-phosphate producing erythrocyte progenitors supports hematopoietic stem cell expansion in fetal liver. Our resource deciphers the temporal waves of hematopoietic development within distinct vascular niches.
2025-06-30 | GSE229427 | GEO
Project description:Reprogramming of Human Fibroblasts into Hematopoietic Progenitors by Fusion With Human Fetal Liver CD34+ Cells (RNA-Seq)
| PRJNA133345 | ENA