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The hemogenic competence of endothelial progenitors is restricted by Runx1 silencing during embryonic development

ABSTRACT: It has now been well established that hematopoietic stem and progenitor cells originate from a specialised subset of endothelium termed hemogenic endothelium (HE) via an endothelial-to-hematopoietic transition. However, the molecular mechanisms determining which endothelial progenitors possess or not this hemogenic potential is currently unknown. In this study, we investigated the changes in hemogenic potential in endothelial progenitors at the early stages of embryonic development. We use a microarray approach to profile the genes regulated between E7.5 and E8.5 embryonic day in the ETV2+FLK1+CD41- compartment.

ORGANISM(S): Mus musculus

PROVIDER: GSE64377 | GEO | 2016/05/31

SECONDARY ACCESSION(S): PRJNA270857

REPOSITORIES: GEO

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The hemogenic competence of endothelial progenitors is restricted by Runx1 silencing during embryonic development

Project description:It has now been well established that hematopoietic stem and progenitor cells originate from a specialised subset of endothelium termed hemogenic endothelium (HE) via an endothelial-to-hematopoietic transition. However, the molecular mechanisms determining which endothelial progenitors possess or not this hemogenic potential is currently unknown. In this study, we investigated the changes in hemogenic potential in endothelial progenitors at the early stages of embryonic development. We use a microarray approach to profile the genes regulated between E7.5 and E8.5 embryonic day in the ETV2+FLK1+CD41- compartment. Cells were sorted based on ETV2::GFP+/FLK1+/CD41- immunophenotype from ETV2::GFP embryos at E7.5 and E8.5 developmental stage in triplicates

2016-05-31 | E-GEOD-64377 | biostudies-arrayexpress

Mesp1 induces a subset of hematopoietic-associated transcription factors in ES cell-derived Flk1+Tie2+ endothelium

Project description:Previously, we reported that the transcription factor Mesp1 promotes the cell fates of cardiomyocytes, smooth muscle, and vascular endothelium. Recently, hematopoietic stem cells (HSCs) were shown to derive from hemogenic endothelium. Since Mesp1 regulates development of endothelium, it potentially could influence gene expression related to hematopoietic development. Our present fate mapping study found that Mesp1-cre efficiently labeled hematopoietic lineages in vivo. This result suggested that Mesp1 might be expressed in progenitors of the hematopoietic system, such as hemogenic endothelium. To test this, we purified Flk1+ Tie2+ endothelium derived from differentiating ES cells with or without Mesp1 induction, and used microarray expression analysis to identify genes strongly up-regulated by Mesp1. Embryonic stem (ES) cells harboring a doxycycline (dox)-inducible Mesp1 gene (A2lox.Mesp1) were differentiated as embryoid bodies for 5 days in the absence (-) or presence (+) of dox from day 2 to day 4. Flk1+Tie2+ endothelial cells were purified by cell sorting for RNA extraction and hybridization on Affymetrix microarrays.

2012-08-02 | E-GEOD-34537 | biostudies-arrayexpress

Gene expression signatures for fractions of E7.5 whole embryos based on Endoglin and Flk-1 markers

Project description:Much remains unknown about the signals that induce early mesoderm to initiate hematopoietic differentiation. Here we show that endoglin (Eng), a receptor for the TGFÎ² superfamily, identifies all cells with hematopoietic fate in the early embryo. These arise in an Eng+Flk1+ mesodermal precursor population at E7.5, a cell fraction also endowed with endothelial potential. In Eng knockout embryos, hematopoietic colony activity and numbers of CD71+Ter119+ erythroid progenitors were severely reduced. This coincided with severely reduced expression of embryonic globin and key BMP target genes including the hematopoietic regulators Scl, Gata1, Gata2 and Msx-1. To interrogate molecular pathways active in the earliest hematopoietic progenitors, we applied transcriptional profiling to sorted cells from E7.5 embryos. Eng+Flk-1+ progenitors co-expressed TGFÎ² and BMP receptors and target genes. Furthermore, Eng+Flk-1+ cells presented high levels of phospho-SMAD1/5, indicating active TGFÎ² and/or BMP signaling. Remarkably, under hematopoietic serum-free culture conditions, hematopoietic outgrowth of endoglin-expressing cells was dependent on TGFÎ² superfamily ligands: BMP4, BMP2, or TGF-Î²1. These data demonstrate that the E+F+ fraction at E7.5 represents mesodermal cells competent to respond to TGFb1, BMP4, or BMP2, shaping their hematopoietic development, and that endoglin is a critical regulator in this process by modulating TGF/BMP signaling. E7.5 pooled embryos (25 litters; 300 embryos approximately) were dissected and 3,000 cells were sorted in triplicate for Eng-Flk1-, Eng-Flk1+, Eng+Flk1+, and Eng+Flk1- fractions. Microarray results were analyzed with GeneSpring GX software.

2012-04-22 | E-GEOD-37515 | biostudies-arrayexpress

Mesp1 induces a subset of hematopoietic-associated transcription factors in ES cell-derived Flk1+Tie2+ endothelium

2012-08-03 | GSE34537 | GEO

RUNX1 and the endothelial origin of blood

Project description:The transcription factor RUNX1 is required in the embryo for formation of the adult hematopoietic system. Here we describe the seminal findings that led to the discovery of RUNX1 and of its critical role in blood cell formation in the embryo from hemogenic endothelium. We also present RNA-Seq data demonstrating that hemogenic endothelial cells in different anatomic sites, which produce hematopoietic progenitors with dissimilar differentiation potentials, are molecularly distinct. Hemogenic endothelial cells and non-hemogenic endothelial cells in the yolk sac are more closely related to each other than either are to hemogenic or non-hemogenic endothelial cells in the major arteries. Thus, a major driver of the different lineage potentials of the committed erythro-myeloid progenitors that emerge in the yolk sac, versus hematopoietic stem cells that originate in the major arteries, is likely to be the distinct molecular properties of the hemogenic endothelial cells from which they are derived. We use bioinformatics analyses to predict signaling pathways active in arterial hemogenic endothelium, several of which are functionally validated pathways including Notch, Wnt, and Hedgehog. We also use a novel bioinformatics approach to assemble transcriptional regulatory networks and predict transcription factors that may be specifically involved in hematopoietic cell formation from arterial hemogenic endothelium, which is the origin of the adult hematopoietic system.

2018-10-05 | GSE103813 | 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

Genome-wide analysis of ETS factor ER71/ETV2 chromatin occupancy

Project description:We discover that ER71/ETV2 initiates hemangiogenic program by activating blood and endothelial cell lineage specifying genes while enhancing FLK1 expression and expanding hemangioblast population. Furthermore, ER71/ETV2 establishes an ETS hierarchy by directly activating Ets genes in hematopoietic and endothelial cell lineage development. As such, ER71/ETV2-initiated blood and endothelial cell program is maintained by ER71/ETV2 downstream ETS factors through an ETS switching mechanism. ChIP-seq analysis of ER71 in differentiated embryonic stem cells

2015-03-30 | E-GEOD-59402 | biostudies-arrayexpress

Genome-wide analysis of ETS factor ER71/ETV2 chromatin occupancy

2015-03-30 | GSE59402 | GEO

Identification of the hemogenic endothelial progenitor and its direct precursor in human pluripotent stem cell differentiation cultures

Project description:Hemogenic endothelium (HE) is the source of HSCs in the developing embryo. In this study we have identified the hemogenic endothelial progenitors and their precursors originating from differentiated H1 cells on OP9 stromal cells. RNA-seq of hemogenic endothelial progenitors and their precursors originating from differentiated H1 cells on OP9 stromal cells.

2012-09-18 | E-GEOD-39661 | biostudies-arrayexpress

Scl specifies hemogenic endothelium and inhibits cardiogenesis via primed enhancers [RNA-seq]

Project description:Scl/Tal1 confers hemogenic competence and prevents cardiomyogenesis in embryonic endothelium. Here we show that Scl both directly activates a broad gene regulatory network required for hematopoietic stem/progenitor cell (HS/PC) development, and represses transcriptional regulators required for cardiogenesis. Cardiac repression occurs during a short developmental window through Scl binding to distant cardiac enhancers that harbor H3K4me1 at this stage. Scl binding to hematopoietic regulators extends throughout HS/PC and erythroid development and spreads from distant enhancers to promoters. Surprisingly, Scl complex partners Gata 1 and 2 are dispensable for hematopoietic versus cardiac specification and Scl binding to the majority of its target genes. Nevertheless, Gata factors co-operate with Scl to activate selected transcription factors to facilitate HS/PC emergence from hemogenic endothelium. These results uncover a dual function for Scl in dictating hematopoietic versus cardiac fate choice and suggest a mechanism by which lineage-specific bHLH factors direct the divergence of competing fates. Examination of Scl and Gata 1 & 2 target genes in ES cell derived day4.75 EB (embryoid body) Tie2+CD31+CD41- endothelial cells

2015-01-01 | E-GEOD-47083 | biostudies-arrayexpress

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