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Metabolomics,Unknown,Transcriptomics,Genomics,Proteomics

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HoxA3 is an apical regulator of hemogenic endothelium

ABSTRACT: 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

ORGANISM(S): Mus musculus

SUBMITTER: Michael Kyba

PROVIDER: E-GEOD-25096 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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HoxA3 is an apical regulator of haemogenic endothelium.

Iacovino Michelina M Chong Diana D Szatmari Istvan I Hartweck Lynn L Rux Danielle D Caprioli Arianna A Cleaver Ondine O Kyba Michael M

Nature cell biology 20101219 1

During development, haemogenesis occurs invariably at sites of vasculogenesis. Between embryonic day (E) 9.5 and E10.5 in mice, endothelial cells in the caudal part of the dorsal aorta generate haematopoietic stem cells and are referred to as haemogenic endothelium. The mechanisms by which haematopoiesis is restricted to this domain, and how the morphological transformation from endothelial to haematopoietic is controlled are unknown. We show here that HoxA3, a gene uniquely expressed in the emb ...[more]

PMID: 21170035

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Epistasis analysis of Runx1 and Gata1 over HoxA3 in hemogenic endothelium

Project description:We observe that HoxA3 represses hematopoieis by the repression of several transcription factors including Runx1 and Gata1. Up regulation of either Runx1 or Gata1 in the presence of HoxA3 reverted the hematopoietic repression. We have performed full genome analysis to determine the molecular signature of hematopoietic development in response to upregulation of Runx1 and Gata1. Endothelial progenitors were sorted from HoxA3 induced EBs, transduced with either control vector (control), Runx1 vector or Gata1 vector. Cells were co-cultured on Op9 for 5 days: in the following conditions: Control, HoxA3 upregulation, HoxA3 + Runx1 upregulation, HoxA3 + Gata1 upregulation in triplicate. After 5 days of culture,transduced cells were sorted (5000 cells) and prepared for microarray.

2010-12-20 | E-GEOD-25079 | biostudies-arrayexpress

Genes regulated by HoxA3 in endothelial and hematopoietic progenitors

Project description:We used a murine ES cell line in which HoxA3 expression is under control of a tetracycline-responsive element and differentiated these cells as embryoid bodies (EBs). Endothelial (Flk-1 VE-cadherin double positive, FV) and hematopoieitc progenitors (c-Kit CD41 double positive, K41) were isolated from differentiated EBs that had been induced for 6 hours by doxycycline (Dox) treatment. Here we show genes regulated upon HoxA3 upregulation (6 hours doxycycline treatment) in hematopoietic and endothelial progenitors.

2010-12-20 | E-GEOD-25080 | biostudies-arrayexpress

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Project description:To investigate how HOXA3 expression in wound tissue alters gene expression to control selective recruitment of bone marrow-derived cell populations, we utilized murine whole genome expression arrays (MEEBO arrays) to identify differentially expressed genes in cutaneous wounds from db/db (diabetic) mice treated with either CMV-HOXA3 or control plasmid. In addition to unwounded control skin, we chose day 4 as the time point to harvest the wounds for RNA isolation, which represents the transition from inflammatory to proliferative phase of wound repair, and precedes the observed differences in BMDC mobilization and recruitment at day 7. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Disease State: cutaneous wound/control skin unwounded skin, wounded skin treated with control plasmid, wounded skin treated with HOXA3

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Dual actions of Meis1 inhibit erythroid progenitor development and sustain general hematopoietic cell proliferation

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HOXA3 functions as the on-off switch to regulate the development of hESC-derived third pharyngeal pouch endoderm through EPHB2-mediated Wnt pathway

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

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