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Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [scRNA-seq]

ABSTRACT: Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [scRNA-seq]

PROVIDER: PRJNA825379 | ENA |

REPOSITORIES: ENA

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Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [scRNA-seq]

Project description:Immune cells must adapt to different environments during an immune response. We studied the adaptation of CD8+ T cells to the intestinal microenvironment and how this process shapes tissue resident CD8+ T cells (TRM) in the gut. CD8+ T cells progressively remodel their transcriptome and surface phenotype as they acquire gut residency, and downregulate mitochondrial gene expression. Human and mouse gut-resident CD8+ T cells have reduced mitochondrial mass, but maintain a viable energy balance to sustain function. We found that the intestinal microenvironment is rich in prostaglandin E2 (PGE2), which drives mitochondrial depolarization in CD8+ T cells. Consequently, they engage autophagy to clear depolarized mitochondria, and enhance glutathione synthesis to scavenge reactive oxygen species (ROS). Impairing PGE2 sensing promotes TRM accumulation, while tampering with autophagy and glutathione negatively impacts the TRM pool. Thus, a PGE2-autophagy-glutathione axis defines the metabolic adaptation of CD8+ T cells to the intestinal microenvironment, to ultimately influence the TRM pool.

2023-11-27 | GSE200567 | GEO

Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [RNA-seq]

2023-11-27 | GSE200566 | GEO

Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment.

Project description:Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment.

| PRJNA825374 | ENA

Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [RNA-seq]

Project description:Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment [RNA-seq]

| PRJNA825380 | ENA

Spleen vs Prostaglandin E2 Treated B cell

Project description:total RNA from mouse (male c57BL/6) spleen labeled with Cy3 vs total RNA from mouse (male c57BL/6) B cells treated with Prostaglandin E2 labeled with Cy5- time course with repeats Keywords: ordered

2003-04-14 | GSE395 | GEO

Prostaglandin E2 (PGE2) Enhances Aged Hematopoietic Stem Cell Function

Project description:Prostaglandin E2 (PGE2) Enhances Aged Hematopoietic Stem Cell Function

| PRJNA729494 | ENA

Enhanced cardiac reprogramming by Inhibition of cyclooxygenase-2/prostaglandin E2/prostaglandin E receptor 4 signaling

Project description:Enhanced cardiac reprogramming by Inhibition of cyclooxygenase-2/prostaglandin E2/prostaglandin E receptor 4 signaling

| PRJNA477816 | ENA

Prostaglandin E2 controls the metabolic adaptation of T cells to the intestinal microenvironment.

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

2023-11-27 | GSE200568 | GEO

Enhanced cardiac reprogramming by Inhibition of cyclooxygenase-2/prostaglandin E2/prostaglandin E receptor 4 signaling

Project description:Direct cardiac reprogramming from fibroblasts can be a promising approach for disease modeling, drug screening, and cardiac regeneration in pediatric and adult patients. However, postnatal and adult fibroblasts are less efficient for reprogramming compared with embryonic fibroblasts, and barriers to cardiac reprogramming associated with aging remain undetermined. In this study, we screened 8,400 chemical compounds, and found that diclofenac sodium (diclofenac), a non-steroidal anti-inflammatory drug, greatly enhanced cardiac reprogramming in combination with Gata4, Mef2c, and Tbx5 (GMT) or GMT plus Hand2. Intriguingly, diclofenac promoted cardiac reprogramming in mouse postnatal and adult tail-tip fibroblasts (TTFs), but not in mouse embryonic fibroblasts (MEFs). Mechanistically, diclofenac enhanced cardiac reprogramming by inhibiting cyclooxygenase-2, prostaglandin E2/prostaglandin E receptor 4, cyclic AMP/protein kinase A, and interleukin 1b pathway, silencing inflammatory and fibroblast programs, which were activated in postnatal and adult TTFs. Thus, anti-inflammation can be a new target for cardiac reprogramming associated with aging.

2019-02-20 | GSE116223 | GEO

Prostaglandin E2 Receptor Subtype EP2- and EP4-regulated Gene Expression Profiling in Human Ciliary Smooth Muscle Cells

Project description:Changes of genome-wide mRNA transcription levels of human ciliary smooth muscle (hCSM) cells were determined by treating hCSM cells in culture with 200 nM of either an prostaglandin E2 receptor subtype EP2 or subtype EP4 selective agonist for 6 hours in comparison to untreated controls. This was followed by competitive hybridization of fluorescent Cy3 or Cy5 labeled cRNA probes derived from the treated versus untreated control total RNA samples onto an Agilent Human Whole Genome Expression oligonucleotide microarray. Log 2 (LN) of the intra-slide ratios (RATIO, PRE_VALUE) of treated versus untreated samples was reported as VALUE in the sample files. Keywords: prostaglandin E2 receptor agonists, subtype EP2, subtype EP4, hCSM

2008-02-24 | GSE10621 | GEO

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