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EP2 receptor modulates macrophage activity for cardiac repair

ABSTRACT: To examine the functional changes of macrophages isolated from wild-type or EP2-KO mice

ORGANISM(S): Mus musculus

PROVIDER: GSE116848 | GEO | 2018/07/11

REPOSITORIES: GEO

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EP2 receptor modulates macrophage activity for cardiac repair

Project description:EP2 receptor modulates macrophage activity for cardiac repair

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MCG 101 tumors implanted on prostaglandin receptor EP2 wildtype and EP2 knockout mice

Project description:Wild type tumor cells, producing high levels of prostaglandin E2 (MCG101, EP2 +/+), were inoculated on EP2 knockout (EP2 -/-) and EP2 wild type (EP2 +/+) mice. Solid tumors were dissected into tumor- and tumor-stroma tissue compartments for RNA expression microarray screening, followed by metabolic pathway analyses. The study aims to evaluate simultaneous gene pathway expressions in separate tissue compartments, such as isolated tumor tissue and tumor stroma respectively.

2022-05-25 | GSE193098 | GEO

Prostaglandin E<sub>2</sub> Receptor 2 Modulates Macrophage Activity for Cardiac Repair.

Project description:Background Prostaglandin E2 has long been known to be an immune modulator. It is released after tissue injury and plays a role in modulating macrophage activities, which are essential for tissue regeneration. However, the involvement of prostaglandin E2 receptor 2 ( EP 2)-dependent regulation of macrophages in postischemic heart is unclear. This study aims to evaluate the role of EP 2 in damaged heart. Methods and Results The effect of EP 2 in postischemic heart was evaluated using EP 2-deficient transgenic mice. We demonstrated that cardiac function was worse after myocardial injury on loss of EP 2. Furthermore, EP 2 deficiency also altered proinflammatory response and resulted in a defect in macrophage recruitment to the injured myocardium. Transcriptome analysis revealed that the expression of erythroid differentiation regulator 1 ( Erdr1) was significantly induced in EP 2-deficient macrophages. Knocking down Erdr1 expression restored migration ability of EP 2-deficient cells both in vitro and in vivo. By using a genetic fate-mapping approach, we showed that abolishment of EP 2 expression effectively attenuated cell replenishment. Conclusions The EP 2-dependent signaling pathway plays a critical role in regulating macrophage recruitment to the injured myocardium, thereby exerting a function in modulating the inflammatory microenvironment for cardiac repair.

| S-EPMC6404869 | biostudies-literature

In vivo response of microglia to Aβ and prostaglandin-E2 EP2 receptor signaling

Project description:Microglia, the innate immune cells of the central nervous system, perform critical inflammatory and non-inflammatory functions to maintain homeostasis and normal neural function. However in Alzheimer’s disease (AD), these beneficial functions become progressively impaired, contributing to synapse and neuron loss and cognitive impairment. The inflammatory cyclooxygenase-PGE2 pathway, including the PGE2 receptor EP2, is implicated in AD development, both in human epidemiology and in transgenic models of AD. To test the transcriptional responses of EP2-deficient microglia to Aβ in vivo, we used mice in which the EP2 receptor is conditionally deleted in microglia using the CD11b-Cre transgene and floxed alleles of the EP2 gene. By injecting these mice with Aβ ICV and isolating microglia from the brains, we have been able to establish the transcriptional response of microglia to Aβ in vivo and test how EP2 deletion in microglia affects this response. 8 month-old C57BL/6 mice, of the genotype CD11b-Cre; EP2+/+ or CD11b-Cre; EP2lox/lox, were injected I.C.V. with either Aβ or vehicle. 48 hours after injection, the mice were sacrificed and transcardially perfused with cold heparinized 0.9% NaCl. Brains were then removed from the mice and pooled, two brains of the same genotype per sample, to ensure adequate cell and RNA yield. The brains were then enzymatically dissociated for microglia isolation using the Neural Tissue Dissociation Kit (P), MACS Separation Columns (LS), and magnetic CD11b Microbeads from Miltenyi Biotec according to the manufacturer's protocol. Immediately after isolating the microglia, RNA was extracted from the cells for microarray analysis.

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In vivo response of microglia to Aβ and prostaglandin-E2 EP2 receptor signaling

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MCG 101 tumors implanted on prostaglandin receptor EP2 wildtype and EP2 knockout mice

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Yersinia pseudotuberculosis strain:EP2/+

Project description:Yersinia pseudotuberculosis EP2/+ Genome sequencing

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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

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Young and aged Myeloid cell treatment with EP2 antagonist PF044

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2020-11-24 | GSE155992 | GEO

Spatial targeting of the prostaglandin receptor EP2 is essential in driving a sustained PGE2-mediated cAMP signaling in the human endometrium

Project description:In a process known as decidualization, progesterone signaling in the human endometrium converges with local cAMP production to drive morphometric and transcriptomic changes that prepare the endometrium for pregnancy. The source of cAMP has been contentious but the prostaglandin PGE2 signaling through EP2, its G-protein coupled receptor, remains a strong candidate. Cells often employ additional receptor regulation to diversify and prolong the cAMP signal and its down-steam effects, most notably through internalization and trafficking of receptors through endosomes. Here, we decidualized cultured endometrial stromal cells for 4-days with PGE2 and MPA (a progestin) and compared transcriptomic profiles with those depleted of either GIPC or APPL1, adaptor proteins involved in trafficking and recycling of EP2 respectively.

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