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Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production [ChIP-seq]

ABSTRACT: ChIP-Seq analyses of GR and PPARa occupancy in mouse E14.5 fetal liver BFU-E cells untreated or treated by DEX with or without GW7647

ORGANISM(S): Mus musculus

PROVIDER: GSE62788 | GEO | 2015/06/08

SECONDARY ACCESSION(S): PRJNA265113

REPOSITORIES: GEO

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Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production [ChIP-seq]

Project description:ChIP-Seq analyses of GR and PPARa occupancy in mouse E14.5 fetal liver BFU-E cells untreated or treated by DEX with or without GW7647 ChIP-Seq on GR and PPAR alpha in purified 10^7 mouse BFU-E cells purified from E14.5 fetal livers with or without treatment of Dexamethasone and/or GW7647

2015-06-08 | E-GEOD-62788 | biostudies-arrayexpress

Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production [RNA-seq]

2015-06-08 | GSE63836 | GEO

Synergism between PPAR? and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production [RNA-seq]

Project description:Analyses of gene expression by RNA-Seq in mouse E14.5 fetal liver burst-forming unit erythroid (BFU-E) cells untreated or treated by dexamethasone (DEX) with or without PPAR? agonist GW7647. RNA-Seq was performed on enriched populations of mouse BFU-E isolated from E14.5 fetal liver, as well as BFU-E enriched cells treated with Dex ± GW7647.

2015-06-08 | E-GEOD-63836 | biostudies-arrayexpress

Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-06-08 | E-GEOD-63837 | biostudies-arrayexpress

Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production

Project description:This SuperSeries is composed of the SubSeries listed below.

2015-06-08 | GSE63837 | GEO

TGF-β inhibitors stimulate red blood cell production by enhancing self-renewal of BFU-E erythroid progenitors

Project description:Erythroid progenitor BFU-Es are so-named based on their ability to generate in methylcellulose culture large colonies of erythroid cells that consist of “bursts” of smaller erythroid colonies derived from the later CFU-E Epo- dependent progenitors. “Early” BFU-E cells forming large BFU-E colonies presumably have higher capacities for self-renewal than do those forming small BFU-E colonies. In order to understand the mechanism underlying this heterogeneity, we conducted single cell transcriptome analysis on BFU-E cells purified from mouse embryos. Our analyses showed that there are two principal subgroups of mouse BFU-E cells and that the type III TGFβ receptor (TβRIII) is a potential marker that distinguishes “early” and “late” BFU-Es. Expression of TβRIII is correlated with that of GATA1, a gene encoding an erythroid transcription factor induced during the BFU-E to CFU-E transition. The mouse and human BFU-E sub populations (TßRIII10%lo) expressing the 10% lowest amount of surface TβRIII are indeed enriched for early BFU-Es, and are significantly more responsive to glucocorticoid stimulation, which promotes BFU-E self-renewal, as compared to the total BFU-E population. The TßRIII10%lo BFU-E subpopulation presumably represents earlier BFU-Es with maximal capacity for self-renewal. Consistent with this notion, signaling by the TGFβ receptor kinases RI and RII increases during the transition from early (TßRIII10%lo) to late (TßRIII10%hi) BFU-Es and then decreases in CFU-E cells. Blocking TGF-β signaling by receptor kinase inhibitors increase TßRIII10%lo BFU-E cell self-renewal and increases total erythroblast production, suggesting the use of this type of drug in treating Epo unresponsive anemias.

2017-01-06 | GSE81505 | GEO

HIF-1synergizes with glucocorticoids to promote BFU-E progenitor self-renewal

Project description:With the aim of finding small molecules that stimulate erythropoiesis earlier than erythropoietin and that enhance CFU-E production, we studied the mechanism by which glucocorticoids increase CFU-E formation. Using BFU-E and CFU-E progenitors purified by a new technique, we demonstrate that glucocorticoids stimulate the earliest (BFU-E) progenitors to undergo limited self-renewal, which increases formation of CFU-E cells > 20-fold. Interestingly, glucocorticoids induce expression of genes in BFU-E cells that contain promoter regions highly enriched for hypoxia-induced factor 1 alpha (HIF1a) binding sites. This suggests activation of HIF1a may enhance or replace the effect of glucocorticoids on BFU-E self-renewal. Indeed, HIF1a activation by a prolyl hydroxylase inhibitor (PHI) synergizes with glucocorticoids and enhances production of CFU-Es 170-fold. Since PHIs are able to increase erythroblast production at very low concentrations of glucocorticoids, PHI-induced stimulation of BFU-E progenitors thus represents a conceptually new therapeutic window for treating Epo-resistant anemia. RNA-Seq was performed on enriched populations of BFU-E, CFU-E and Ter119+ as well as BFU-E enriched cells treated with Dex and DMOG

2010-12-21 | E-GEOD-26086 | biostudies-arrayexpress

Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production

Project description:Synergism between PPARα and glucocorticoid receptor signaling promotes self-renewal of BFU-E erythroid progenitors and increases red cell production

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System Analysis of The Functional Cross-Talk Between PPARα, LXR and FXR in HepaRG Liver Cells

Project description:The purpose of the present study was to explore in liver cells the connectivity that operates between three nuclear receptors in the liver, LXR, FXR, and PPARa, all three known to act on lipid and glucose metabolism, and also on inflammation. The human cell line HepaRG was selected for its proximity to human primary hepatocytes. Global gene expression of differentiated HepaRG cells was assessed after 4 hours and 24 hours of exposure to GW3965 (LXR agonist), GW7647 (PPARα agonist), and GW4064 and CDCA (FXR synthetic and natural agonist, respectively).

2019-06-27 | GSE124053 | GEO

HIF-1synergizes with glucocorticoids to promote BFU-E progenitor self-renewal

2010-12-21 | GSE26086 | GEO

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