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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

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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.

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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

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2023-10-24 | PXD044040 | Pride

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