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Effect of GFI1B ectopic expression in the hematopoietic or endothelial commitment of human iPSC derived CD34+CD43-CD73- hemogenic endothelium (HE)

ABSTRACT: Effect of GFI1B ectopic expression in the hematopoietic or endothelial commitment of human iPSC derived CD34+CD43-CD73- hemogenic endothelium (HE)

PROVIDER: PRJNA1032643 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR26539594_1.fastq.gz	Fastqsanger.gz
	SRR26539594_2.fastq.gz	Fastqsanger.gz
	SRR26539595_1.fastq.gz	Fastqsanger.gz
	SRR26539595_2.fastq.gz	Fastqsanger.gz
	SRR26539596_1.fastq.gz	Fastqsanger.gz

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Effect of GFI1B ectopic expression in the hematopoietic or endothelial commitment of human iPSC derived CD34+CD43-CD73- hemogenic endothelium (HE)

Project description:In this study we focused on unrevealing the role of major transcriptional factor GFI1B and its cofactor, LSD1 in human endothelial to hematopoietic transition (EHT). We applied irreversible LSD1 inhibitor (GSK-LSD1) to healthy iPSC lines. Interestingly, LSD1 inhibited healthy lines which showed complete absence of hematopoietic cell output, did not showed detection of GFI1B expression, suggesting a timed transcriptional program. In order to test this hypothesis, we ectopically expressed GFI1B in the uncommitted HE cells, leading to downregulation of endothelial genes and an upregulation of hematopoietic genes, including GATA2, KIT, RUNX1 and SPI1.

2024-12-18 | GSE246386 | GEO

Expression data of human ES cells-derived CD34+CD43+CD45low cells (hemogenic endothelium-like cells) expanded upon overexpression of Sox17

Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells and hematopoietic cells enhances expansion of hemogenic endothelium-like cells. Human ES cells were differentiated for 6 days, 8 days or 12 days in EBs, then CD34+CD43-CD45- endothelial cells, CD34+CD43+CD45- pre-hematopoietic progenitor cells (HPCs) or CD34+CD43+CD45+ HPCs were isolated by fluorescence activated cell sorting (FACS) and subjected to a microarray analysis.M-cM-^@M-^@Some samples were plated onto OP9 cells after the isolation by FACS, and transduced with the 4OH-tamoxifen-inducible 1M-CM-^WFLAG-tagged Sox17-ERT retrovirus. The cells were cultured with 4OH-tamoxifen. CD34+CD43+CD45low hemogenic endothelium-like cells expanded by Sox17-ERT were collected by magnetic-activated cell sorting (MACS) and subjected to a ChIP-chip analysis.

2012-12-14 | E-GEOD-37348 | biostudies-arrayexpress

ChIP-on-chip data from human ES cells-derived CD34+CD43+CD45low cells (hemogenic endothelium-like cells) overexpressing 3xFLAG-Sox17-ERT

Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells enhances expansion of hemogenic endothelium-like cells. Human ES cells were differentiated for 6 days in EBs, then CD34+CD43-CD45- endothelial cells were isolated, plated onto OP9 cells, and transduced with the 4OH-tamoxifen (4OHT)-inducible 3×FLAG-tagged Sox17-ERT retrovirus. The cells were seeded on OP9 stromal cells and cultured in the presence of 4OH-tamoxifen. At day 27 of the co-culture with OP9 cells, CD34+CD43+CD45low hemogenic endothelium-like cells overexpressing Sox17-ERT were collected by CD34 magnetic-activated cell sorting (MACS) and subjected to a ChIP-chip analysis.

2012-12-14 | E-GEOD-37528 | biostudies-arrayexpress

Expression data of human ES cells-derived CD34+CD43+CD45low cells (hemogenic endothelium-like cells) expanded upon overexpression of Sox17

Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells and hematopoietic cells enhances expansion of hemogenic endothelium-like cells.

2012-12-14 | GSE37348 | GEO

ChIP-on-chip data from human ES cells-derived CD34+CD43+CD45low cells (hemogenic endothelium-like cells) overexpressing 3xFLAG-Sox17-ERT

Project description:Overexpression of transcription factor Sox17 in human ES cells-derived endothelial cells enhances expansion of hemogenic endothelium-like cells.

2012-12-14 | GSE37528 | GEO

HoxA3 is an apical regulator of hemogenic endothelium

Project description:This SuperSeries is composed of the following subset Series: GSE25079: Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium GSE25080: Genes regulated by HoxA3 in endothelial and hematopoietic progenitors Refer to individual Series

2010-12-20 | E-GEOD-25096 | biostudies-arrayexpress

Hemogenic Endothelium transcriptome along the timeline of hESC differentiation

Project description:The differentiation of human embryonic stem cells to hematopoietic lineages initiates with the specification of hemogenic endothelium, a transient specialized endothelial precursor of all blood cells.Unfortunately, absence of hemogenic endothelium-specific markers as well as lack of consensus in the timing of hemogenic potential analysis and methodologies used to study the hematopoietic potential of this precursor prevents reaching clear and definite conclusions. Here, we demonstrate that the hemogenic potential of the endothelium precursor population sharply decline over the course of the differentiation process. Poly(A) RNA-sequencing on CD31+CD144+ population at day 6, day 8 and day 10 of EB diffferentiation with or without the addition of cytokines. Comparasion with hematopoietic committed population CD31+CD144- from day 10 of EB differentiation.

2018-10-25 | GSE109648 | GEO

mRNA profiles of CD43++c-kit+, CD43+c-kit- and CD43-c-Kit- AML1-ETO9a murine leukemic bone marrow cells

Project description:We discovered a spontaneous differentiation path characterized by CD43 and c-Kit in the AE9a murine model, where the leukemia-initiating potential is lost while leukemic cells display features of erythroid maturation. Therefore, we sorted out CD43++c-Kit+, CD43+c-Kit- and CD43-c-Kit- AE9a leukemic cells for RNA-sequencing analyses to determine the underlying transcriptome.

2022-10-03 | GSE186040 | GEO

Induction of a hemogenic program in mouse fibroblasts

Project description:Definitive hematopoiesis emerges during embryogenesis via an endothelial-to-hematopoietic transition. We attempted to induce this process in mouse fibroblasts by screening a panel of factors for hemogenic activity. We identified a combination of four transcription factors, Gata2, Gfi1b, cFos, and Etv6 that efficiently induces endothelial-like precursor cells with the subsequent appearance of hematopoietic cells. The precursor cells express a human CD34 reporter, Sca1 and Prominin1 within a global endothelial transcription program. Emergent hematopoietic cells possess nascent/specifying hematopoietic stem cell gene expression profiles and cell surface phenotypes. After transgene silencing and reaggregation culture, the specified cells generate hematopoietic colonies in vitro. Thus, we have shown that a simple combination of transcription factors is sufficient to induce a complex, dynamic and multi-step developmental program in vitro. These findings provide insights into the specification of definitive hemogenesis and a platform for future development of patient-specific stem/progenitor cells as well as more differentiated blood products. mRNA-seq profiling on populations generated after transduction with Gata2, Gfi1b, cFos and Etv6 at day 20 and day 35.

2013-06-13 | E-GEOD-47497 | biostudies-arrayexpress

Cooperative Transcription Factor Induction Mediates Hemogenic Reprogramming

Project description:During development, hematopoietic stem/progenitor cells (HSPCs) arise from specialized endothelial cells by a process termed endothelial-to-hematopoietic transition (EHT). The genetic program driving human HSPC emergence remains largely unknown. We previously reported that the generation of hemogenic precursor cells from mouse fibroblasts recapitulates developmental hematopoiesis. Here, we demonstrate that human fibroblasts can be reprogrammed into hemogenic cells by the same transcription factors. Induced cells display dynamic EHT transcriptional programs, generate hematopoietic progeny, possess HSPC cell surface phenotype and repopulate immunodeficient mice for three months. Mechanistically, GATA2 and GFI1B interact and co-occupy a cohort of targets. This cooperative binding is reflected by engagement of open enhancers and promoters, initiating silencing of fibroblast genes and activating the hemogenic program. However, GATA2 displays dominant and independent targeting activity during the early phases of reprogramming. These findings shed light on the processes controlling human HSC specification and support generation of reprogrammed HSCs for clinical applications.

2018-12-04 | GSE51025 | GEO

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