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

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

PROVIDER: PRJNA269185 | ENA |

REPOSITORIES: ENA

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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 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 [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

2015-06-08 | GSE62788 | 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

PPARα mouse liver cistrome

Project description:Autophagy is an evolutionally conserved catabolic process that recycles nutrients upon starvation and maintains cellular energy homeostasis1-3. Its acute regulation by nutrient sensing signaling pathways is well described, but its longer-term transcriptional regulation is not. The nuclear receptors PPARα and FXR are activated in the fasted or fed liver, respectively4,5. Here we show that both regulate hepatic autophagy. Pharmacologic activation of PPARα reverses the normal suppression of autophagy in the fed state, inducing autophagic lipid degradation, or lipophagy. This response is lost in PPARα knockout (PPARα-/-) mice, which are partially defective in the induction of autophagy by fasting. Pharmacologic activation of the bile acid receptor FXR strongly suppresses the induction of autophagy in the fasting state, and this response is absent in FXR knockout (FXR-/-) mice, which show a partial defect in suppression of hepatic autophagy in the fed state. PPARα and FXR compete for binding to shared sites in autophagic gene promoters, with opposite transcriptional outputs. These results reveal complementary, interlocking mechanisms for regulation of autophagy by nutrient status. Mouse liver PPARα cistromes in fed 8-week-old male WT or PPARα KO mice treated with or without its synthetic agonist ligand GW7647twice a day were generated by deep sequencing in quadruplicate using illumina

2014-09-27 | E-GEOD-61817 | biostudies-arrayexpress

PPAR-? and glucocorticoid receptor synergize to promote erythroid progenitor self-renewal.

Project description: Not available

| S-EPMC4498266 | biostudies-literature

Transcriptional profiling of PPARα-/- and CREB3L3-/- livers reveals disparate regulation of hepatoproliferative and metabolic functions of PPARα

Project description:Peroxisome Proliferator-Activated receptor α (PPARα) and cAMP-Responsive Element Binding Protein 3-Like 3 (CREB3L3) are transcription factors involved in the regulation of lipid metabolism in the liver. The aim of the present study was to characterize the interrelationship between PPARα and CREB3L3 in regulating hepatic gene expression. Male wildtype, PPARα-/-, CREB3L3-/- and combined PPARα/CREB3L3-/- mice were subjected to a 16-hour fast or 4 days of ketogenic diet. Whole genome expression analysis was performed on liver samples. Under conditions of overnight fasting, the effects of PPARα ablation and CREB3L3 ablation on plasma triglyceride, plasma β-hydroxybutyrate, and hepatic gene expression were largely disparate, and showed only limited interdependence. Gene and pathway analysis underscored the importance of CREB3L3 in regulating (apo)lipoprotein metabolism, and of PPARα as master regulator of intracellular lipid metabolism. A small number of genes, including Fgf21 and Mfsd2a, were under dual control of PPARα and CREB3L3. By contrast, a strong interaction between PPARα and CREB3L3 ablation was observed during ketogenic diet feeding. Specifically, the pronounced effects of CREB3L3 ablation on liver damage and hepatic gene expression during ketogenic diet were almost completely abolished by the simultaneous ablation of PPARα. Loss of CREB3L3 influenced PPARα signalling in two major ways. Firstly, it reduced expression of PPARα and its target genes involved in fatty acid oxidation and ketogenesis. In stark contrast, the hepatoproliferative function of PPARα was markedly activated by loss of CREB3L3. These data indicate that CREB3L3 ablation uncouples the hepatoproliferative and lipid metabolic effects of PPARα. Overall, except for the shared regulation of a very limited number of genes, the roles of PPARα and CREB3L3 in hepatic lipid metabolism are clearly distinct and are highly dependent on dietary status.

2019-01-23 | GSE121096 | GEO

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