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Prostaglandin E2 inhibits pro-fibrotic function of human pulmonary fibroblasts by disrupting Ca2+-signaling

ABSTRACT: Prostaglandin E2 inhibits pro-fibrotic function of human pulmonary fibroblasts by disrupting Ca2+-signaling

PROVIDER: PRJNA487726 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7750590.fastq.gz	Fastqsanger.gz
	SRR7750600.fastq.gz	Fastqsanger.gz
	SRR7750591.fastq.gz	Fastqsanger.gz
	SRR7750601.fastq.gz	Fastqsanger.gz
	SRR7750592.fastq.gz	Fastqsanger.gz

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Prostaglandin E2 inhibits pro-fibrotic function of human pulmonary fibroblasts by disrupting Ca2+-signaling

Project description:Purpose: Identification of gene expression in human lung fibroblasts, including analysis of impact of IPF (Idiopathic Pulmonary Fibrosis) as well as TGFβ stimulation, with particular emphasis on prostanoid receptors and related pathways. Methods: Truseq stranded mRNA sequencing, via Illumina Hiseq 4000. Single reads, 75bp, ~25 million reads per sample. Quantification of gene expression in TPM using Kallisto, followed by Tximport. mRNA isolated via Qiagen RNeasy kit, with on-column DNase1 digestion. Results: Quantification of gene expression in primary human lung fibroblasts, including quantification of prostanoid GPCRs.

2019-03-01 | GSE119007 | GEO

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

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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

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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

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Prostaglandin E2-mediated T cell suppression requires expression of hydroxyprostaglandin dehydrogenase in regulatory T cells.

Project description:Prostaglandins are involved in maintaining tissue integrity under homeostatic conditions. However, in chronic inflammation and cancer prostaglandins have been linked to immune deviation including strong suppression of effector T-cell function. Yet, the molecular mechanisms underlyingimmunosuppression and the cell types involved are only purely understood. Here, we show for the first time that Treg cells are the critical cellular component exerting immunosuppressive effects in prostaglandin E2 (PGE2)-rich environments. Hydroxyprostaglandin dehydrogenase (HPGD), which catabolizes PGE2 into immunosuppressive metabolites, is the critical molecular link between prostaglandin accumulation, increased Treg-cell function and avoidance of tissue destruction.

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Microglial response to Aβ and prostaglandin-E2 EP4 receptor activation

Project description:A persistent and non-resolving inflammatory response to accumulating Aβ peptide species is a cardinal feature in the development of Alzheimer's disease (AD). In response to accumulating Aβ peptide species, microglia, the innate immune cells of the brain, generate a toxic inflammatory response that accelerates synaptic and neuronal injury. Many pro-inflammatory signaling pathways are linked to progression of neurodegeneration. However, endogenous anti-inflammatory pathways capable of suppressing Aβ-induced inflammation represent a relatively unexplored area. Here we hypothesized that signaling through the prostaglandin-E2 (PGE2) EP4 receptor potently suppresses microglial inflammatory responses to Aβ42 peptides. In cultured microglial cells, EP4 stimulation attenuated levels of Aβ42-induced inflammatory factors and potentiated phagocytosis of Aβ42. Microarray analysis was performed and demonstrated that EP4 stimulation broadly opposed Aβ42-driven gene expression changes in microglia, with enrichment for targets of IRF1, IRF7, and NF-κB transcription factors.

2014-04-25 | GSE55627 | GEO

Mast Cells Control Lung Type 2 Inflammation via Prostaglandin E2-Driven Soluble ST2.

Project description:Mast Cells Control Lung Type 2 Inflammation via Prostaglandin E2-Driven Soluble ST2.

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