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PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells [scRNA-seq]

ABSTRACT: PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells [scRNA-seq]

PROVIDER: PRJNA1117063 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29198181_1.fastq.gz	Fastqsanger.gz
	SRR29198181_2.fastq.gz	Fastqsanger.gz
	SRR29198182_1.fastq.gz	Fastqsanger.gz
	SRR29198182_2.fastq.gz	Fastqsanger.gz
	SRR29198183_1.fastq.gz	Fastqsanger.gz

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PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells

Project description:PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells

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PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells

Project description:The formation of antigen-specific memory CD8+ T cells is one of the most important features of the adaptative immune system, allowing the establishment of long-term protection against secondary infections. Although emerging evidence suggests that metabolic reprogramming is crucial for memory T cell differentiation and survival, the underlying mechanisms that drive metabolic rewiring needed for memory T cells remain unclear. Here, we found that the nuclear receptor peroxisome proliferator-activated receptor-beta/delta (PPARβ/δ) was upregulated to instruct the metabolic reprogramming, including downregulation of aerobic glycolysis and the promotion of oxidative metabolism and fatty acid oxidation, that occurs during the transition toward the establishment of central memory CD8+ T cells. Mechanistically, the exposure to interleukin-15 (IL-15) and expression of T cell factor 1 (TCF1) could coordinately activated the PPARβ/δ pathway during acute viral infection and chronic antigen exposure contexts, counteracting apoptosis induced by antigen clearance and metabolic stress. Together, our work indicates that PPARβ/δ is a master metabolic regulator orchestrating the metabolic reprogramming required for the establishment of a metabolic profile favorable for T cells longevity.

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PPARβ/δ-orchestrated metabolic reprogramming supports the formation and maintenance of memory CD8+ T cells [scRNA-seq]

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Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

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Genome-wide maps of H3K27ac, PPARβ/δ and Pol II localization in HUVECs

Project description:H3K27Ac is one of the expressed enhancer markers, PPARβ/δ is a transcription factor and Pol II (RNA polymerase II) is an enzyme which catalyzes the transcription of DNA to synthesize precursors of mRNA and most snRNA and microRNA. These genomic localization in endothelial cells is unknown in endothelial cells. This time, we established a new antibody for H3K27ac, PPARβ/δ and Pol II and performed ChIP-seq to identify H3K27ac, PPARβ/δ and Pol II binding site in whole genome manner under PPARβ/δ agonist and/or hypoxia. We used chromatin immunoprecipitation with deep sequencing (ChIP-seq) of HUVECs treated with PPARβ/δ agonist (GW501516 100nM) and/or hypoxia (1%O2) for 24hours, then H3K27ac, PPARβ/δ and Pol II binding regions were identified. Normoxia and DMSO was used as a control condition. HUVECs were used within the first 6 passages.

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Expression data of HUVEC cells after PPARβ/δ agonist and/or hypoxia treatment

Project description:Recently the role of PPARβ/δ in angiogenesis has been revealed, and we hypothesized that the crosstalk between hypoxia and PPARβ/δ on endothelial cells may exsist. To elucidate the interaction between two signalings, we report the comprehensive change of transcripts induced by PPARβ/δ agonist (GW501516) and/or hypoxia. We used microarray analysis of HUVECs treated with PPARβ/δ agonist (GW501516) and/or hypoxia (1% O2) for 24-hours, and we identified a group of consistently up- or down-regulated genes. HUVECs were used within the first 6 passages. HUVECs were treated with PPARβ/δ agonist (GW501516) at a concentration of 100 nM and/or hypoxia (1% O2) for 24-hours. Same concentration of DMSO was used as a control sample, and as to the oxgen, normoxia was used as a control condition.

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