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Transcriptome profile of murine bone marrow-derived macrophages treated with 15d-PGJ2 or 15d-PGJ2-PC

ABSTRACT: Purpose: The goal of this study is to investigate the alteration of gene expression pattern induced by 15d-PGJ2 or 15d-PGJ2-PC in BMDMs. Method: BMDMs obtained from C57BL/6 mice were treated with 15d-PGJ2, 15d-PGJ2-PC or media control for 6h. Then RNA sequence was generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 13 million sequence reads per sample to the mouse genome and identified about 14,500 transcripts in the macrophage mRNAs. Among them, 719 and 286 genes were differentially expressed in 15d-PGJ2 and 15d-PGJ2-PC group respectively. Conclusions: Deoxy-A2/J2-IsoP-PC are a novel series of oxidation products we identified in atherosclerotic plaques. 15d-PGJ2-PC is a representative compound of these oxidation products we chemically synthesised. Using RNA-seq technology, we provided 15d-PGJ2-PC induced gene expression profile and could contribute to study the roles of these novel oxidation products in the atherosclerosis.

ORGANISM(S): Mus musculus

PROVIDER: GSE85931 | GEO | 2016/08/24

SECONDARY ACCESSION(S): PRJNA339783

REPOSITORIES: GEO

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Transcriptome profile of murine bone marrow-derived macrophages treated with 15d-PGJ2 or 15d-PGJ2-PC

Project description:Purpose: The goal of this study is to investigate the alteration of gene expression pattern induced by 15d-PGJ2 or 15d-PGJ2-PC in BMDMs. Method: BMDMs obtained from C57BL/6 mice were treated with 15d-PGJ2, 15d-PGJ2-PC or media control for 6h. Then RNA sequence was generated by using the Illumina system. Results: Using an optimized data analysis workflow, we mapped about 13 million sequence reads per sample to the mouse genome and identified about 14,500 transcripts in the macrophage mRNAs. Among them, 719 and 286 genes were differentially expressed in 15d-PGJ2 and 15d-PGJ2-PC group respectively. Conclusions: Deoxy-A2/J2-IsoP-PC are a novel series of oxidation products we identified in atherosclerotic plaques. 15d-PGJ2-PC is a representative compound of these oxidation products we chemically synthesised. Using RNA-seq technology, we provided 15d-PGJ2-PC induced gene expression profile and could contribute to study the roles of these novel oxidation products in the atherosclerosis. mRNA profiles of BMDMs from C57B/L6 mice were generated by deep sequencing, in triplicate, using Illumina.

2016-08-24 | E-GEOD-85931 | biostudies-arrayexpress

Identification of 15d-PGJ2 target proteins

Project description:15-deoxy-delta12,14-prostaglandin J2 (15d-PGJ2) is an endogenous anti-inflammatory lipid derived from PGD2. One potential mechanism for its activity is the covalent modification of cellular proteins, via a reactive alpha,beta-unsaturated carbonyl group in its cyclopentenone ring, which in turn alters protein function. In order to identify the target proteins covalently modified by 15d-PGJ2 in human aortic endothelial cell (EC), EC were treated with biotinylated-15d-PGJ2, the modified proteins extracted by Neutravidin affinity-purification and the proteins were identified by LTQ Orbitrap mass spectrometer.

2015-04-26 | PXD000006 | Pride

Electrophilic lipid mediator 15-deoxy-Δ12,14-prostaglandin J2 modifies glucocorticoid signaling via receptor SUMOylation

Project description:Cortisol, the central stress hormone in humans, activates the glucocorticoid receptor (GR). Anti-inflammatory effects are the most important pharmaceutical effects mediated by the GR. Inasmuch as electrophilic cyclopentenone prostaglandin 15-deoxy-Δ12,14-prostaglandin J2 (15d-PGJ2) has potent anti-inflammatory properties and activates the SUMOylation pathway, we have investigated the effect of 15d-PGJ2 on glucocorticoid signaling and receptor SUMOylation. To this end, we studied isogenic HEK293 cells expressing either wild-type GR or SUMOylation-defective GR. Interestingly, 15d-PGJ2 triggered SUMO-2/3 modification in the primary SUMOylation sites of the GR. Gene expression profiling and pathway analyses indicate that 15d-PGJ2 inhibits GR signaling in a genome-wide fashion that is significantly dependent on the GR SUMOylation sites. Chromatin immunoprecipitation assays showed that the repressive effect of 15d-PGJ2 on GR target gene expression occurs in parallel with the inhibition of receptor binding to the target gene chromatin. Furthermore, depletion of the sole SUMO E2 conjugase UBC9 from HEK293 cells confirmed the involvement of active SUMOylation in the regulatory process. Taken together, our data indicate that GR SUMOylation modulates the glucocorticoid signaling during acute cell stress. Our data also suggest that GR SUMOylation modulates crosstalk of the glucocorticoid signaling with other transcription factors that are responsive to cell stress.

2014-06-30 | GSE54087 | GEO

Electrophilic lipid mediator 15-deoxy-M-NM-^T12,14-prostaglandin J2 modifies glucocorticoid signaling via receptor SUMOylation

Project description:Cortisol, the central stress hormone in humans, activates the glucocorticoid receptor (GR). Anti-inflammatory effects are the most important pharmaceutical effects mediated by the GR. Inasmuch as electrophilic cyclopentenone prostaglandin 15-deoxy-M-NM-^T12,14-prostaglandin J2 (15d-PGJ2) has potent anti-inflammatory properties and activates the SUMOylation pathway, we have investigated the effect of 15d-PGJ2 on glucocorticoid signaling and receptor SUMOylation. To this end, we studied isogenic HEK293 cells expressing either wild-type GR or SUMOylation-defective GR. Interestingly, 15d-PGJ2 triggered SUMO-2/3 modification in the primary SUMOylation sites of the GR. Gene expression profiling and pathway analyses indicate that 15d-PGJ2 inhibits GR signaling in a genome-wide fashion that is significantly dependent on the GR SUMOylation sites. Chromatin immunoprecipitation assays showed that the repressive effect of 15d-PGJ2 on GR target gene expression occurs in parallel with the inhibition of receptor binding to the target gene chromatin. Furthermore, depletion of the sole SUMO E2 conjugase UBC9 from HEK293 cells confirmed the involvement of active SUMOylation in the regulatory process. Taken together, our data indicate that GR SUMOylation modulates the glucocorticoid signaling during acute cell stress. Our data also suggest that GR SUMOylation modulates crosstalk of the glucocorticoid signaling with other transcription factors that are responsive to cell stress. Total RNA isolated from isogenic HEK293 cell lines stably expressing either wild-type GR (wtGR) or SUMOylation-defective GR (GR3KR) treated with 100 nM of dexamethasone (dex) in the presence or absence of 5 M-BM-5M 15d-PGJ2 for 6h. All conditions are performed in triplicate

2014-06-30 | E-GEOD-54087 | biostudies-arrayexpress

Mus musculus

Project description:Transcriptome profile of murine bone marrow-derived macrophages treated with 15d-PGJ2 or 15d-PGJ2-PC

| PRJNA339783 | ENA

Prostaglandin J2 alters gene expression patterns and 26S proteasome assembly in human neuroblastoma cells

Project description:Many neurodegenerative disorders are characterized by two pathological hallmarks: progressive loss of neurons and occurrence of inclusion bodies containing ubiquitinated proteins. The mechanisms responsible for these pathological features remain elusive. Inflammation may be critical to neurodegeneration associated with ubiquitin-protein aggregates. We previously showed that prostaglandin J2 (PGJ2), one of the endogenous products of inflammation, induces neuronal death and accumulation of ubiquitinated proteins into distinct aggregates. We now report that temporal microarray analysis of human neuroblastoma SK-N-SH cells treated with PGJ2 revealed changes relevant to neurodegeneration. PGJ2 triggered a “repair” response including increased expression of heat shock, protein folding, stress and cellular defense genes. PGJ2 also decreased expression of DNA repair genes and increased expression of apoptotic genes. Overtime pro-death responses prevailed over pro-survival responses, leading to cellular demise. Furthermore, PGJ2 increased the expression of proteasome and other ubiquitin-proteasome pathway genes. This increase failed to overcome PGJ2-inhibition of 26S proteasome activity. Ubiquitinated proteins are degraded by the 26S proteasome, shown here to be the most active proteasomal form in SK-N-SH cells. We demonstrate that PGJ2 impairs 26S proteasome assembly, which is an ATP-dependent process. Interestingly, PGJ2 is known to perturb mitochondrial function, which could be critical to the observed 26S proteasome disassembly and suggest a crosstalk between mitochondrial and proteasomal impairment. In conclusion neurotoxic products of inflammation, such as PGJ2, may play a role in neurodegenerative disorders associated with the aggregation of ubiquitinated proteins by impairing 26S proteasome activity and inducing a chain of events that culminates in neuronal cell death. Keywords: Drug response time course

2006-06-01 | GSE4329 | GEO

Protein modifications in plasma during SARS-CoV-2 infection

Project description:Although the COVID-19 pandemic has ended, it is important to understand the pathology of severe SARS-CoV-2 infection associated with respiratory failure and high mortality. In this study, a proteomics approach using nano-HPLC-MS/MS (QExactive HF) was used to compare the plasma proteome of COVID-19 survivors (COVID-19; n=10) and deceased individuals (CovDeath; n=10) with that of healthy individuals (Ctr; n=10). The effects of SARS-CoV-2 infection on the alteration of plasma proteins by lipid peroxidation products such as 4-hydroxynonenal (4-HNE), malondialdehyde (MDA) and 15-deoxy-12,14-prostaglandin J2 (15d-PGJ2) were also examined. The results suggest that the development of COVID-19 strongly alters the expression of proteins involved in the regulation of exocytosis and platelet degranulation. These changes were most pronounced in the CovDeath group. In addition, a significant increase in proteins modified with reactive aldehydes was observed in all patients. In the COVID-19 and CovDeath groups, the levels of 4-HNE adducts increased 2- and 3-fold, respectively, whereas MDA adducts increased 7- and 2.5-fold, respectively. Signaling kinases and proinflammatory proteins were particularly affected by these modifications, and the amount of 4-HNE modifications confirmed previous findings on the relevance of 4-HNE in disease pathogenesis and lethal outcome. Protein adducts with 15d-PGJ2 were increased 2.5-fold in COVID-19 patients, including modifications of proteins such as p53 and STAT3, whereas CovDeath showed a decrease of approximately 60% compared with Ctr. It can be assumed that the observed changes in protein expression and modification in COVID-19 are unlikely to be used as prognostic biomarkers because they are also present in the other inflammatory diseases. However, larger studies may prove that the extent and the nature of protein modifications in plasma may be a predictor of the course of SARS-CoV-2 infection.

2023-10-24 | PXD044040 | Pride

Gene alterations by PPAR-gamma agonists in human colorectal adenocarcinoma HCT-116 cells

Project description:We examined the alternation of gene expression by MCC-555, rosiglitazone (RGZ) and 15-deoxy-Δ12, 14-prostaglandin J2 (PGJ2) in human colorectal adenocarcinoma HCT-116 cells. Keywords: effects of PPAR-gamma agonists

2008-06-10 | GSE9183 | GEO

Mass spectrometry imaging of phosphatidylcholine metabolism in lungs administered with therapeutic surfactants and isotopic tracers

Project description:<p>Mass spectrometry imaging (MSI) visualises molecular distributions throughout tissues but is blind to dynamic metabolic processes. Here, MSI with high mass resolution together with multiple stable isotope labelling provided spatial analyses of phosphatidylcholine (PC) metabolism in mouse lungs. Dysregulated surfactant metabolism is central to many respiratory diseases. Metabolism and turnover of therapeutic pulmonary surfactants were imaged from distributions of intact and metabolic products of an added tracer, universally 13C-labelled dipalmitoyl PC (U[13C]DPPC). The parenchymal distributions of newly synthesised PC species were also imaged from incorporations of methyl-D9-choline. This dual labelling strategy demonstrated both lack of inhibition of endogenous PC synthesis by exogenous surfactant and location of acyl chain remodelling processes acting on the U[13C]DPPC-labelled surfactant, leading to formation of polyunsaturated PC lipids. This ability to visualise discrete metabolic events will greatly enhance our understanding of lipid metabolism in diverse tissues, and has potential application to both clinical and experimental studies. </p>

2020-10-30 | MTBLS2075 | MetaboLights

ChIPseq to profile CDK9 and Hes1 occupancy in bone marrow-derived macrophages from C57BL/6 mice

Project description:We characterized the CDK9 and Hes1 occupancy on gene loci in conditions of unstimuated and LPS stimualtion in BMDMs BMDMs were left untreated or stimulated with LPS for 1 hour. CDK9 or Hes1 ChIP was performed and the DNA products were subject to ChIPseq

2016-06-13 | E-GEOD-77334 | biostudies-arrayexpress

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