Transcription profiling of mouse IL-1b responses in receptor-reconstituted AcP-deficient neurons
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
SUBMITTER: Chris Russell
PROVIDER: E-GEOD-16104 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:The purpose was to determine AcP- and AcPb-dependent gene responses to IL-1 by virally-reconstituting AcP-deficient mouse embryonic cortical neurons with CD25 (control), full length AcP, AcPb or the combination of both. A control population was transduced with a CD25-expressing virus. Half the samples were stimulated with IL-1-beta for four hours, RNA was analyzed by microarray.
2009-07-01 | GSE16104 | GEO
Project description:IRAK-4 is an essential component of the signal transduction complex downstream of the IL-1- and Toll-like receptors. Though regarded as the first kinase in the signaling cascade, the role of IRAK-4 kinase activity versus its scaffold function is still controversial. In order to investigate the role of IRAK-4 kinase function in vivo, knock-in mice were generated by replacing the wild type IRAK-4 gene with a mutant gene encoding kinase deficient IRAK-4 protein (IRAK-4 KD). Analysis of embryonic fibroblasts and macrophages obtained from IRAK-4 KD mice with a number of experimental techniques demonstrated that they greatly lack responsiveness to stimulation with IL-1b or a Toll-like receptor 7 (TLR7) agonist. One of the techniques used, microarray analysis, identified IRAK-4 kinase-dependent IL-1b response genes in mouse embryonic fibroblasts and revealed that the induction of IL-1b-responsive mRNAs was largely ablated in IRAK-4 KD cells. In summary, our results suggest that IRAK-4 kinase activity plays a critical role in IL-1R/TLR7-mediated induction of inflammatory responses. Experiment Overall Design: The response of mouse embryonic fibroblasts from WT and IRAK4 kinase dead animals to stimulation with IL-1b at two time points was determined. There were 12 samples in total, 6 from WT and 6 from IRAK4 kinase dead cells; for each strain there were 3 conditions: growth for 4 hours without stimulation (the strain-specific control), growth for 1 hour with stimulation, and growth for 4 hours with stimulation; for each condition there were two biological replicates.
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Project description:Chondrocytes undergo changes to their protein translational capacity during osteoarthritis progression, but a study of how disease-relevant signals affect chondrocyte protein translation at the transcriptome level has not previously been performed. In this study we describe how the inflammatory cytokine IL-1B rapidly affects protein translation in the chondrosarcoma cell line SW1353. Using ribosome profiling we demonstrate that IL-1B induced altered translation of inflammatory-associated transcripts through differential translation and the use of multiple open reading frames. Proteomic analysis of the cellular layer and the conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. We have produced combined ribosome profiling and proteomic datasets which provide a valuable resource in understanding the processes that are occuring during cytokine stimulation of chondrocytic cells.
2019-07-11 | PXD012985 | Pride
Project description:Chondrocytes undergo changes to their protein translational capacity during osteoarthritis progression, but a study of how disease-relevant signals affect chondrocyte protein translation at the transcriptomic level has not previously been performed. In this study we describe how the inflammatory cytokine IL-1B rapidly affects protein translation in the chondrocytic cell line SW1353. Using ribosome profiling we demonstrate that IL-1B induced altered translation of inflammatory-associated transcripts, as well as a number of ribosome-associated transcripts, through differential translation and the use of multiple open reading frames. Proteomic analtsis of the cell layer and conditioned media of these cells identified that proteins which were differentially translated were most readily detected in the secretome. We have produced combined ribosome profiling and proteomic datasets which provide a valuble resource in understanding the processes that are occoring during cytokine stimulation of chondrocytic cells.
2019-09-27 | PXD011740 | Pride
Project description:Cytokines have been shown to play a key role in the destruction of beta cells. In the rat insulinoma cell line (INS-1ab) overexpressing pancreatic duodenum homeobox 1 (Pdx1) increases sensitivity to Interleukin 1b (IL-1b). To elucidate mechanisms of action underlying Pdx1 driven potentiation of beta-cell sensitivity to IL-1β, we performed a microarray analysis of INS-1ab cells with and without Pdx1 overexpression exposed to IL-1β between 2h and 24h. INS-1ab cells were cultured with or without 500 ng/ml doxycycline (+/- DOX). After 24 h, 40 ng/ml IL-1b was either added or not (+/- IL-1b). Cells were harvested either 2h, 4h, 6h, 12h or 24h after addition of IL-1b. Four biological replicates for each of the eight groups.
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Project description:IL-1 plays an important role in atherosclerosis, and alters expression of a number of genes involved in atherosclerotic plaque development and progression. Smooth muscle cells play important roles in atherosclerotic plaque formation and stability, so this study was undertaken to determine the global effects of IL-1b on gene expression in smooth muscle cells in vitro. Cultured rat aortic smooth muscle cells were treated with IL-1b (2.5 ng/mL) or vehicle (0.1% BSA) for 24 hours prior to harvest.
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Project description:This program aims at identifying the lung gene signature associated with inflammation and emphysema in IL-1b-Tg mouse COPD model to facilitate understanding of the disease mechanism and therapeutic compound testing The lung profiling data was analyzed by identifying genes that were up- and down-regulated at selected p value and fold change in the lungs of IL-1b-Tg mice treated with doxycycline (to induce IL-1b transgene) compared to the corresponding water-treated controls.
2013-03-22 | E-GEOD-38075 | biostudies-arrayexpress
Project description:IL-1B is an important cytokine that is often found to be up-regulated during osteoarthritic and rheumatoid joint diseases. It is viewed as a catabolic factor, inducing enzymes that allow for the degradation of the cartilage extracellular matrix and also has essential roles as an autocrine and paracrine factor in fibronectin fragment-mediated degradation. It can also reduce the synthesis of the major cartilage components, type II collagen and aggrecan. On the other hand, IL-1B also has the ability to induce the growth and morphogenic factor BMP-2. During joint diseases, IL-1B is synthesized by both synovial cells and chondrocytes. Addition of IL-1 biological antagonists such as IL-1 receptor antagonists can suppress cartilage degradation in vitro. Thus, the production of IL-1B could act as the first step in mediating a cascade of other mediators in cartilage which could be relevant to the fate of the cartilage. In order to obtain a global picture of the effect of IL-1B production on human adult articular chondrocytes, we analyzed changes in gene expression induced by IL-1B by microarray analysis. We found that IL-1B has a diverse effect on gene expression profile in chondrocytes. One of the predominant responses that we observed in adult human articular chondrocytes on exposure to IL-1B is a dramatic increase in a large set of chemokines and other genes related to the inflammatory cascade. Keywords: Gene response to IL-1B (10 ng/ml) Cartilage was obtained from adult human tissue donors with above the knee amputations due to chondrosarcoma or traumatic injury or from autopsy. Chondrocytes were isolated following established protocols, maintained in high density, and treated with IL-1B (10 ng/ml). Chondrocytes treated with buffer only served as the untreated control. The experiment was carried out in duplicate. Total RNA was extracted from these chondrocytes, labeled with fluorophores (Cy3 or Cy5) and analyzed for expression changes using the Human Operon/Qiagen v3.0 oligonucleotide array. The analysis was repeated with the fluorophore dyes exchanged between the untreated and experimental RNAs.
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