Expression data from endothelial cells isolated from IL-33 knock-out and wildtype rats
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
PROVIDER: GSE121577 | GEO | 2023/12/31
REPOSITORIES: GEO
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Project description:IL-33 is a nuclear cytokine from the IL-1 family that plays important roles in health and disease.Under healthy conditions, IL-33 is constitutively expressed to high levels in the nucleus of producing cells in various human and mouse tissues. The extracellular function of IL-33 cytokine has been well documented, but it remains unclear whether intracellular nuclear IL-33 has additional functions in the nucleus. Here, we used a global proteomic approach based on quantification of 5000 individual proteins by high-resolution mass spectrometry to compare the extracellular and intracellular roles of IL-33 in primary human endothelial cells, a major source of IL-33 protein in human tissues. Large-scale analysis of protein expression was performed either after stimulation of the cells with the IL-33 mature form IL-3395-270 (during 6h or 24h) or after siRNA knockdown of intracellular IL-33 (two experiments, each with a different pool of distinct siRNAs, noted siRNA1 and siRNA2). In each case, proteins were fractionated by 1D SDS-PAGE in 12 gel bands, and label-free quantitative analysis was performed. The present dataset corresponds to the stimulation of human endothelial cells with IL-3395-270 during 6h (IL33_6) or 24h (IL33_24). Cells cultured in the absence of IL-33 were used as control (CTil33). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 9 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 108 raw files.
2016-10-10 | PXD004117 | Pride
Project description:IL-33 is a nuclear cytokine from the IL-1 family that plays important roles in health and disease. Under healthy conditions, IL-33 is constitutively expressed to high levels in the nucleus of producing cells in various human and mouse tissues. The extracellular function of IL-33 cytokine has been well documented, but it remains unclear whether intracellular nuclear IL-33 has additional functions in the nucleus. Here, we used a global proteomic approach based on quantification of 5000 individual proteins by high-resolution mass spectrometry to compare the extracellular and intracellular roles of IL-33 in primary human endothelial cells, a major source of IL-33 protein in human tissues. Large-scale analysis of protein expression was performed either after stimulation of the cells with the IL-33 mature form IL-3395-270 (during 6h or 24h) or after siRNA knockdown of intracellular IL-33 (two experiments, each with a different pool of distinct siRNAs, noted siRNA1 and siRNA2). In each case, proteins were fractionated by 1D SDS-PAGE in 12 gel bands, and label-free quantitative analysis was performed. The present dataset contains the files for the two experiments of knockdown of endogenous nuclear IL-33 expression: - RNA silencing strategy 1. Knockdown of endogenous nuclear IL-33 expression was performed with a pool of four distinct siRNAs (Dharmacon ON-TARGETplus SMARTpool IL-33 siRNAs) that have been specifically modified for efficient silencing of the target gene with reduced off-target effects. Cells transfected with these siRNA duplexes (si1) were compared with those transfected with the provided controls (CTsi1). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 6 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 72 raw files. - RNA silencing strategy 2. The second knockdown strategy was based on the use of an independent pool of three siRNAs targeting IL-33, predesigned by another provider using new and critical siRNA design rules (Sigma MISSION Predesigned Il-33 siRNAs based on Rosetta siRNA design algorithm). Cells transfected with these siRNA duplexes (si2) were compared with those transfected with the provided controls (CTsi2). Three independent biological replicates (noted _A, _B, _C) were prepared and analyzed for each condition, leading to 6 different samples. Each of them was fractionated into 12 gel bands analyzed by nanoLC-MS/MS, leading to 72 raw files.
2016-10-12 | PXD004141 | Pride
Project description:Pulmonary arterial hypertension (PAH) is characterized by severe obstruction of small pulmonary arteries and concomitant high pulmonary arterial pressure, resulting in progressive right ventricular failure. Previously, we demonstrated that long-term interleukin (IL)-33 administration in mice induced severe occlusive arterial hypertrophy in the lung, which was mediated by group 2 innate lymphoid cells (ILC2s). In response to IL-33, ILC2s accumulated around blood vessels and produced IL-5, leading to perivascular eosinophil recruitment. In this study, we further characterized IL-33-induced pulmonary arterial hypertrophy. We first demonstrated that long-term IL-33 administration caused an increase in the right ventricular pressure. In IL-33 deficient mice, pulmonary arterial hypertrophy mediated by eggs of Schistosoma mansoni (S. mansoni) was attenuated, accompanied with partial reduction in ILC2s, eosinophils and CD4+ T cells. In addition, proteomic analysis revealed dramatic changes in urine samples from mice treated with IL-33 or S. mansoni eggs. Resistin like alpha (RELM), a pulmonary hypertension-related molecule, in the urine was commonly detected in both treatments. Large amounts of RELM were observed in the lung from IL-33-treated mice. These observations support that IL-33-induced pulmonary arterial hypertrophy is a useful model to study the mechanism underlying development of PAH and expolar biomarkers to indicate the onset of PAH.
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Project description: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.
2013-03-05 | GSE37624 | GEO
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
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
Project description:Interleukin-33 (IL-33) is a novel member of the IL-1 family of cytokines that plays diverse roles in the regulation of immune responses. IL-33 exerts its effects by binding to a heterodimeric receptor complex consisting of interleukin-1 receptor like 1 (IL1RL1) and an accessory receptor protein IL-1RAcP resulting in the production and release of proinflammatory cytokines. A detailed understanding of the signaling pathways activated by IL-33 remains elusive. To elucidate IL-33 mediated signaling, we performed a global quantitative phosphoproteomic analysis using stable isotope labeling by amino acids in cell culture. Employing anti-phosphotyrosine antibodies and titanium dioxide-based enrichment strategies, we identified 6,207 phosphorylation sites mapping to 2,013 phosphoproteins of which more than 185 phosphosites are regulated by IL-33 stimulation. Our findings will greatly expand the understanding of IL-33 signaling and provide novel therapeutic targets for IL-33/IL-33R-associated diseases in humans.
2015-01-29 | PXD000984 | Pride
Project description:ILC2 cells are a newly described cell type whose biology and contribution to disease are poorly understood. ILC2 cells are activated by allergens, viral infection, and/or epithelial damage via IL-33 and IL-25. ILC2 cells require IL-2, IL-7, IL-25 and IL-33 for their survival and expansion. In mice, ILC2s produce multiple mediators primarily associated with type 2 inflammation (IL-13, IL-5, IL-4, IL-6, IL-9, IL-10, GM-CSF, amphiregulin). ILC2 cells may contribute to the pathology of asthma through multiple mediators that include IL-13-independent pathways. Our goal is to compare transcriptional profiles of IL-33- or IL-25-activated ILC2 cells from blood to characterize these cells and to identify marker(s) that can be utilized to detect them in human tissue. ILC2 cells (Lineage negative, CRTH2+, CD161+, CD127+) were purified from human blood of 5 different donors by flow cytometry. The ILC2 yield ranged from 20,000 to 165,000 cells per donor (0.001-0.008% WBC). Purified ILC2s were expanded in vitro in the presence of IL-2, IL-7, IL-33 and IL-25 (each at 50 ng/ml) for 7-10 days. Expanded cells maintained the ILC2 phenotype (Lineage negative, CRTH2+, CD161+, CD127+). The cells were rested for 2 days in the presence of 1 ng/ml IL-2 and IL-7 and then treated in the presence of 1 ng/ml IL-2 and IL-7 with either media control, IL-25 (50 ng/ml), IL-33 (50 ng/ml), and/or TSLP (50 ng/ml) in combination, for 6 or 24 hours. Whole RNA was isolated via the RNeasy kit (Qiagen). Stratagene Universal Human Reference RNA was used as the reference.
2013-12-31 | E-GEOD-45458 | biostudies-arrayexpress
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Project description:Glioma cells response Interleukin-33 (IL-33) [microarray]
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