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EED in the Polycomb Repressive Complex 2 Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages

ABSTRACT: EED in the Polycomb Repressive Complex 2 Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages

PROVIDER: PRJNA982709 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR24894154_1.fastq.gz	Fastqsanger.gz
	SRR24894154_2.fastq.gz	Fastqsanger.gz
	SRR24894155_1.fastq.gz	Fastqsanger.gz
	SRR24894155_2.fastq.gz	Fastqsanger.gz
	SRR24894156_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

EED in the Polycomb Repressive Complex 2 Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages

Project description:To avoid exaggerated inflammation and injury, host cells adapt to become hypo-responsive or “tolerance” in response to successive exposure to stimuli. Such tolerized response is a part of innate immune memory which is mainly regulated via epigenetics changes and metabolic reprograming. Polycomb repressive complex 2 (PRC2) mediates the transcriptional repression by catalyzing histone H3 lysine 27 trimethylation (H3K27me3) but little is known about the roles of PRC2 in tolerant macrophages. We examined the impact of PRC2 components, EED and Ezh2, on lipopolysaccharide (LPS)-induced tolerant macrophages. In Eed KO macrophages, not only the significant reduction in H3K27me3, but also the augmentation of an active histone mark, H3K27Ac. Upon EED deletion but not Ezh2, macrophages exhibited attenuated pro-inflammatory cytokines productions (TNF-α and IL-6) in LPS-tolerant cells. In addition, LPS tolerant Eed KO macrophages exhibited low glycolytic activity rather than its littermate wild-type control. RNA-Seq analyses revealed that most of differentially expressed genes are involved in oxidative phosphorylation and TGF-β signaling. Alteration of H3K27me3 and H3K27ac in the regulatory regions of some of these genes were validated. These results indicated that PRC2 via EED epigenetically suppresses these genes in response to LPS re-exposure and lacking PRC2 activity results in hypo-responsive to LPS re-stimulation. Therefore, we provide strong evidences that PRC2 via EED mediates LPS tolerance in macrophages by epigenetically suppressing proinflammatory responses with the link to dysregulated metabolic pathway.

2023-06-20 | GSE234655 | GEO

A Polycomb Group Protein EED Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages via Metabolic Flux and TGF-/Runx3 Axis

Project description:To avoid exaggerated inflammation and injury, innate immune cells adapt to become hypo-responsive or “tolerance” in response to successive exposure to stimuli, which is a part of innate immune memory. Polycomb repressive complex 2 (PRC2) mediates the transcriptional repression by catalyzing histone H3 lysine 27 trimethylation (H3K27me3) but little is known about its roles in tolerant macrophages. We examined the impact of deletion of the PRC2 component, EED on lipopolysaccharide (LPS)-induced tolerant macrophages. In Eed KO macrophages, significant reduction in global H3K27me3 and increased global active histone mark, H3K27ac was observed. Eed KO macrophages exhibited dampened pro-inflammatory cytokine productions (TNF-α and IL-6) while increased non-tolerizeable genes upon LPS tolerance. In addition, LPS tolerized Eed KO macrophages exhibited lower glycolytic activity than its wild-type control. RNA-Seq analyses revealed that the hallmarks of hypoxia, TGF-β, and Wnt/β-catenin signaling were enriched in LPS tolerized Eed KO macrophages. Among the upregulated genes, EED was found to be associated with the Runx3 promoter. Silencing Runx3 in Eed KO macrophages partially rescued the dampened pro-inflammatory response during LPS tolerance. Enrichment of H3K27me3 was decreased in genes that are upregulated in Eed KO LPS tolerance macrophages. Taken together, our results provided mechanistic insight into how the PRC2 via EED regulates LPS tolerance in macrophages via TGF-/Runx3 axis by epigenetically silencing genes that play a central role during LPS tolerance.

2024-12-31 | GSE249512 | GEO

A Polycomb Group Protein EED Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages via Metabolic Flux and TGF-/Runx3 Axis

Project description:A Polycomb Group Protein EED Epigenetically Regulates Responses in Lipopolysaccharide Tolerized Macrophages via Metabolic Flux and TGF-/Runx3 Axis

| PRJNA1049422 | ENA

A polycomb group protein EED epigenetically regulates responses in lipopolysaccharide tolerized macrophages

Project description: Not available

| S-EPMC11606203 | biostudies-literature

Bulk RNA-seq of Colonic Epithelia from EED and EED/Satb2 Double Knockout Mice

Project description:To understand the polycomb repressive complex 2 (PRC2) function, we genetically deleted EED, which inactivated PRC2, in adult intestine and colon using (VillinCreER-T2;EEDf/f).

2021-10-05 | GSE180013 | GEO

The JAK2-STAT pathway epigenetically regulates tolerized genes during the first encounter to bacterial antigens

Project description:The JAK2-STAT pathway epigenetically regulates tolerized genes during the first encounter to bacterial antigens

| PRJNA668134 | ENA

The Central Role of EED in the Orchestration of Polycomb Group Complexes

Project description:Polycomb Repressive Complexes 1 and 2 (PRC1 and 2) play a critical role in the epigenetic regulation of transcription during cellular differentiation, stem cell pluripotency, and neoplastic progression1-3. Here we show that the Polycomb group protein EED, a core component of PRC2, physically interacts with and functions as part of the PRC1 complex. Components of PRC1 and PRC2 compete for EED binding. EED functions to recruit PRC1 to H3K27me3 loci and enhances PRC1 mediated H2A ubiquitin E3 ligase activity. Taken together, we uncover the integral role of EED as an epigenetic exchange factor coordinating the activities of PRC1 and 2. EED, uH2A, RING1A, RING1B, BMI1 and H3K27Me3 ChIP-seq in EED stable knockdown and control Scramble DU145 prostate cancer cell line

2014-01-23 | E-GEOD-42566 | biostudies-arrayexpress

Polycomb repressive complex 1 (PRC1) role in skin epithelium development [Epi Eed cKO]

Project description:Polycomb repressive complex 1 (PRC1) role in skin epithelium development [Epi Eed cKO]

| PRJNA446059 | ENA

The JAK2-STAT pathway epigenetically regulates tolerized genes during the first encounter to bacterial antigens [array]

Project description:The JAK2-STAT pathway epigenetically regulates tolerized genes during the first encounter to bacterial antigens [array]

| PRJNA668108 | ENA

EED orchestration of heart maturation through interaction with HDACs is H3K27me3-independent

Project description:In proliferating cells, where most Polycomb repressive complex 2 (PRC2) studies have been performed, gene repression is associated with PRC2 trimethylation of H3K27 (H3K27me3). However, it is uncertain whether PCR2 writing of H3K27me3 is mechanistically required for gene silencing. Here we studied PRC2 function in postnatal mouse cardiomyocytes, where the paucity of cell division obviates bulk H3K27me3 rewriting after each cell cycle. EED (Embryonic Ectoderm Development) inactivation in the postnatal heart (Eed CKO ) caused lethal dilated cardiomyopathy. Surprisingly, gene upregulation in Eed CKO was not coupled with loss of H3K27me3. Rather, the activating histone mark H3K27ac increased. EED interacted with histone deacetylases (HDACs) and enhanced their catalytic activity. HDAC overexpression normalized Eed CKO heart function and expression of derepressed genes. Our results uncovered a non-canonical, H3K27me3-independent EED repressive mechanism that is essential for normal heart function. Our results further illustrate that organ dysfunction due to epigenetic dysregulation can be corrected by epigenetic rewiring.

2017-04-14 | GSE73771 | GEO

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