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Transcriptional response of confluent human umbilical vein endothelial cells to stimulation with the related cytokines interleukin-1b or interleukin-33.

ABSTRACT: The similar response of endothelial cells to exogenous IL-33 or IL-1β prompted us to compare the genome-wide transcription profile of confluent human umbilical vein endothelial cell (HUVEC) cultures after 4 hours exposure to IL-33 or IL-1β. Analysis of these data revealed a striking similarity in the transcriptional response to the two cytokines.

ORGANISM(S): Homo sapiens

PROVIDER: GSE37624 | GEO | 2013/03/05

SECONDARY ACCESSION(S): PRJNA162379

REPOSITORIES: GEO

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Transcriptional response of confluent human umbilical vein endothelial cells to stimulation with the related cytokines interleukin-1b or interleukin-33.

Project description:The similar response of endothelial cells to exogenous IL-33 or IL-1M-NM-2 prompted us to compare the genome-wide transcription profile of confluent human umbilical vein endothelial cell (HUVEC) cultures after 4 hours exposure to IL-33 or IL-1M-NM-2. Analysis of these data revealed a striking similarity in the transcriptional response to the two cytokines. Pooled HUVEC from 10 donors were seeded 10.000 cells/cm2 and cultured for 4 days before stimulation for 4 hours with IL-1M-NM-2 0.5 ng/ml or IL-33 50 ng/ml. Total RNA was isolated using the RNeasy Mini Kit (Qiagen) according to instructions of the manufacturer. Microarrays were performed using an Illumina Human6 v2 Expression Beadchip, and the raw data was pre-processed by IlluminaM-bM-^@M-^Ys BeadStudio software V2. The expression service was provided by Helse SM-CM-8r-M-CM-^Xst/University of Oslo Microarray Core Facility, a member of the Norwegian Microarray Consortium supported by the functional genomics program (FUGE) at the Research Council of Norway.

2013-03-05 | E-GEOD-37624 | biostudies-arrayexpress

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Determination of the molecular mechanism of IL33 on glioma cells Since IL-33 is known to associate with chromatin and regulate transcriptional activity and that nuclear expression of IL-33 increases glioma progression, we determined Nuclear IL-33 regulates the expression and secretion of inflammatory cytokines in glioma cells. Using these parameters 340 genes were induced by the ectopic expression of IL-33 and an additional 377 genes were downregulated. Gene ontology terms over-represented in the genes induced by IL-33 include three major clusters that associate with cytokine activity and inflammation

2020-08-21 | GSE153486 | GEO

A proteomic landscape of the spatiotemporal influence of Interleukin-33 (IL-33) in monocytes

Project description:Interleukin-33 (IL-33), a member of the IL-1 superfamily cytokines, is an endogenous danger signal and a nuclear-associated cytokine. It is one of the essential mediators of both innate and adaptive immune responses. Aberrant IL-33 signaling has been demonstrated to play a defensive role against various infectious and inflammatory diseases. Although the signaling responses mediated by IL-33 have been previously reported, the temporal signalingdynamicsare yet to be explored. Towards this end,we applied quantitative temporal phosphoproteomics analysis to elucidate pathways and proteins induced by IL-33 in THP1 monocytes. Employing TMT labeling-based quantitation and titanium dioxide (TiO2)-based phosphopeptide enrichment strategy followed by mass spectrometry analysis, we identified 14,515 phosphorylation sites mapping to 4,174 proteins across (0 min to 240 mins)time points.

2022-02-16 | PXD028673 | Pride

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:To validate the modulation of inflammatory genes by ectopic IL-33, we performed Gene expression analysis using the nCounter Mouse v2 Inflammation Panel. This result validated a significant increase in a number of anti-inflammatory cytokines in the IL-33+ xenografts that were absent in the DNLS xenografts

2020-08-21 | GSE153488 | GEO

Knockdown of interleukin-33 in human fibroblasts

Project description:Interleukin (IL)-33 is a cytokine that appears to mediate fibrosis by signaling via its receptor ST2 (IL-33R/IL1RL1). It is also, however, a protein that after synthesis is sorted to the cell nucleus, where it appears to affect chromatin folding. Here we describe a novel role for nuclear IL-33 in regulating the fibroblast phenotype in murine kidney fibrosis driven by unilateral ureteral obstruction. Transcriptional profiling of IL-33-deficient kidneys 24h after ligation revealed enhanced expression of fibrogenic genes and enrichment of gene sets involved in extracellular matrix formation and remodeling. These changes relied on intracellular effects of IL-33, because they were not reproduced by treatment with a neutralizing antibody to IL-33 that prevents IL-33R/ST2L receptor signaling nor were they observed in IL33R/ST2-deficient kidneys. To further explore the intracellular function of IL-33, we established transcription profiles of human fibroblasts, observing that knockdown of IL-33 skewed the transcription profile from an inflammatory towards a myofibroblast phenotype, reflected in higher levels of COL3A1, COL5A1 and transgelin protein, as well as lower expression levels of IL6, CXCL8, CLL7 and CCL8. In conclusion, our findings suggest that nuclear IL-33 in fibroblasts dampens the initial profibrotic response until persistent stimuli, as enforced by UUO, can override this protective mechanism.

2020-05-06 | GSE149917 | GEO

Glioma cells response Interleukin-33 (IL-33) [microarray]

Project description:Glioma cells response Interleukin-33 (IL-33) [microarray]

| PRJNA642838 | ENA

Dataset of spatiotemporal influences of interleukin IL-1 family cytokine: Interleukin-33 on cellular signal transduction pathways

Project description:Interleukin-33 (IL-33) is a member of the IL-1 family of cytokines that play a central role in the regulation of immune responses. IL-33 signaling, from the early signaling events triggered by the ligand-activated receptor to result in activation of early and late signaling events, such as proteome changes. In this study, THP1 (monocyte) cell line model was stimulated with IL-33 (50 ng/ml) for varying duration (5, 10, 15, 30, 40, 60, 120 and 240 mins). We carried out in-depth proteomic analysis using high-resolution LC-MS/MS. Our analysis resulted in the identification of 64,030 peptides corresponding to 7947 protein groups. Differentially regulated proteins identified in this study could be targeted for developing an inflammatory immune response.

2022-02-17 | PXD024385 | Pride

Subconfluent and confluent aortic endothelial cells

Project description:Gene expression changes in subconfluent mouse aortic endothelial cells were compared with confluent endothelial cells. Compartmental analysis showed coordinater response in several endothelial-specific functions and organelles (endoplasmic reticulum, Golgi, lysosomes, peroxisomes) which were downregulated, and upregulation of the microtubular system and proliferation. Keywords = endothelium Keywords = confluent Keywords = subconfluent Keywords = organelles Keywords: other

2005-01-20 | GSE1576 | GEO

Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

Project description:Mouse immune cells response Interleukin-33 (IL-33) [nanostring]

| PRJNA642836 | ENA

Interleukin 1b triggers catabolism via a central nervous system-mediated pathway in mice and rat

Project description:Hypothalamic interleukin-1 beta (IL-1β) production is induced in multiple inflammatory diseases associated with muscle catabolism. To determine whether IL-1β signaling in the CNS plays a role in the muscle wasting of inflammatory disease, we examined the ability of intracerebroventricular (ICV) IL-1β injection at pathophysiologically relevant concentrations, to generate catabolic changes in skeletal muscle. Changes in gene expression associated with these catabolic changes were monitored using gene expression exon arrays. 28 samples were analyzed. The following comparisons were made: 6 groups were defined on the basis of treatment and time. Differences between groups were assesed by one way-ANOVA. P values were corrected for multiple comparisons using the Benjamini Hochberg correction at a false discovery rate of 1%. Probes were considered that showed a 1.75 fold or greater up or down regulation at any of the three timepoints.

2011-11-03 | E-GEOD-26766 | biostudies-arrayexpress

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