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Transcription profiling of human IFN-Gamma treated keratinocytes

ABSTRACT: An experiment comparing control versus IFN-g treated skin cells (one design factor on two levels). To evaluate the biological and the experimental variability, the following experimental design was planned as shown in Figure 1: "Control" and "IFN-g stimulated" keratinocytes were cultured in triplicate using three individual petri Ã10 culture dishes and RNA was independently extracted from each cultured replicate. For each RNA sample, cRNA synthesis was performed in triplicate and each cRNA pool was hybridized to an Affymetrix U133 Gene Chip.

ORGANISM(S): Homo sapiens

SUBMITTER: Anton Petrov

PROVIDER: E-GEOD-1132 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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The Global Error Assessment (GEA) model for the selection of differentially expressed genes in microarray data.

Mansourian Robert R Mutch David M DM Antille Nicolas N Aubert Jerome J Fogel Paul P Le Goff Jean-Marc JM Moulin Julie J Petrov Anton A Rytz Andreas A Voegel Johannes J JJ Roberts Matthew-Alan MA

Bioinformatics (Oxford, England) 20040514 16

<h4>Motivation</h4>Microarray technology has become a powerful research tool in many fields of study; however, the cost of microarrays often results in the use of a low number of replicates (k). Under circumstances where k is low, it becomes difficult to perform standard statistical tests to extract the most biologically significant experimental results. Other more advanced statistical tests have been developed; however, their use and interpretation often remain difficult to implement in routine ...[more]

PMID: 15145801

Similar Datasets

IFN-Gamma keratinocytes

Project description:An experiment comparing control versus IFN-g treated skin cells (one design factor on two levels). To evaluate the biological and the experimental variability, the following experimental design was planned as shown in Figure 1: "Control" and "IFN-g stimulated" keratinocytes were cultured in triplicate using three individual petri Æ10 culture dishes and RNA was independently extracted from each cultured replicate. For each RNA sample, cRNA synthesis was performed in triplicate and each cRNA pool was hybridized to an Affymetrix U133 Gene Chip. Keywords: ordered

2004-09-01 | GSE1132 | GEO

Mi-2β knockout enhanced response of B16F10 cells to IFN-γ

Project description:Mi-2β-knockout and non-target control B16F10 cell lines were created using a clustered regular interspaced short palindromic repeats/CRISPR-associated protein 9 (CRISPR/Cas9) system. Total RNA was extracted from Mi-2β knockout and control B16F10 cells, which were treated with IFN-γ (10ng/mL) for 24 hours, for microarray assay. The experimental group cells were cultured in triplicate. The experiment was comprised of 6 Mouse Gene 2.0 ST arrays.

2023-05-23 | GSE151640 | GEO

The effects of terbutaline or GW9508 on TNF-alpha and IFN gamma (TNF-alpha + IFN gamma) stimulation by HaCaT

Project description:G-protein coupled receptors (GPCRs) have diverse roles in physiological processes, including immunity. Gs-coupled GPCRs increase while Gi-coupled ones decrease intracellular cAMP. Previous studies suggest that, in epithelial cells, Gs-coupled GPCRs enhance whereas Gi-coupled GPCRs suppress pro-inflammatory immune responses. In order to examine the issue, we chose beta2 adrenergic receptor and GPR40 as representatives of Gs- and Gi- coupled GPCRs, respectively, and examined their effects on TNF-alpha and IFN-gamma-(TNF-alpha + IFN-gamma) induced gene expression by HaCaT. We used microarrays to detail the global changes of gene expression induced by a beta2 adrenergic receptor agonist terbutaline or GPR40 agonist GW9508 pre-treatment in TNF-alpha + IFN-gamma - stimulated HaCaT cells. HaCaT cells were pre-treated with terbutaline or GW9508, TNF-alpha + IFN-gamma were then added, and cultured for another 24 h. Cells were then used for RNA extraction and hybridization on Affymetrix microarrays. We sought to clarify changes in gene expression after 1) TNF-alpha + IFN-gamma, 2) TNF-alpha + IFN-gamma + terbutaline, and 3) TNF-alpha + IFN-gamma + GW9508 treatment. To this end, we set 4 groups of samples; 1) unstimulated group, 2) TNF-alpha + IFN-gamma-stimulated group, 3) TNF-alpha + IFN-gamma + terbutaline-stimulated group, and 4) TNF-alpha + IFN-gamma + GW9508-stimulated group. In each group, HaCaT cells were stimulated in triplicate wells (n=3).

2010-12-01 | E-GEOD-20297 | biostudies-arrayexpress

RNA-Seq analysis of mouse group 2 innate lymphoid cells (ILC2s) cultured with IL-33, IFN-g, and IL-27

Project description:Purpose: We found that IFN-g and IL-27 had suppressive effects on ILC2s cultured with IL-33. The goal of this study is to clarify the expressions of RNA induced by IFN-g and IL-27 in ILC2s. Methods: ILC2s were isolated from fat-asociated lymphid clusters (FALC) of wild-type mice. They were cultured with IL-33 (10ng/ml), IL-33 + IFN-g (10ng/ml), or IL-33 + IL-27 (10ng/ml) for 48hrs. RNA was isolated by Allprep DNA/RNA Micro Kit (QIAGEN), and cDNA libraries were prepared by TruSeq RNA Sample Preparation kits v2 (Illumina) according to the manufacturerâs low sample protocol. A HiSeq 1500 system (Illumina) was used for 50 single-end bases (50SE)ãsequencing. Results: Sequenced reads were trimmed for adaptor sequence, and masked for low-complexity or low-quality sequence, then mapped to the reference genome (mm9) using Bowtie2 v2.1.0 and TopHat2 v2.0.8. The transcript abundances were estimated as FPKM (fragments per kilobase of exon million fragments mapped) value using Cufflinks v2.1.1. We found that both IL-27 and IFN-g upregulated the expression of STAT1 and IRF1 which are regulated downstream of IFN-g receptor signaling, but there was no difference in the expression of GATA3, a critical transcription factor for ILC2 functions. Conclusions: Our study represents the detailed differences of RNA expressions by RNA-seq technology. RNA-Seq analysis of ILC2s cultured with IL-33 (10ng/ml), IL-33 + IFN-g (10ng/ml), or IL-33 + IL-27 (10ng/ml) for 48hrs.

2015-10-30 | E-GEOD-73272 | biostudies-arrayexpress

Analysis of transcriptional differences after IFN-beta (IFN-b) or IFN-lambda (IFN-l) treated human mid-gestation chorionic villus explants

Project description:Purpose: Treatment of midgestation chorionic villus explants with recombinant IFN-b leads to morphological changes including formation of syncitial knots. However, treatment of explants with IFN-l, which is constitutively expressed by syncytiotrophoblasts, is not sufficient to cause these same changes. To understand the different transcriptional changes induced by IFN-b and IFN-l and underlying cause of these morphological changes, we performed RNAsequencing after these different treatments. Methods: Chorionic villi of 18-21 gestation week placentas were dissected. Explants were cultured in DMEM F/12 with 1000 U recombinant IFN-b or 1000U recombinant IFN-l for 24 hours. RNA was then isolated from explants, and RNAsequencing was performed to assess transcriptional changes. Results/ Conclusions: IFN-b but not IFN-l induces interferon stimulated genes (ISGs) in mid gestation chorionic villus explants.

2017-12-31 | GSE104348 | GEO

Suppression of IFN-induced transcription underlies IFN defects generated by activated Ras/MEK in human cancer cells

Project description:Certain oncolytic viruses exploit activated Ras signalling in order to replicate in cancer cells. Constitutive activation of the Ras/MEK pathway is known to suppress the effectiveness of the interferon (IFN) antiviral response, which may contribute to Ras-dependent viral oncolysis. Here, we identified 10 human cancer cell lines (out of 16) with increased sensitivity to the anti-viral effects of IFN-α after treatment with the MEK inhibitor U0126, suggesting that the Ras/MEK pathway underlies their reduced sensitivity to IFN. To determine how Ras/MEK suppresses the IFN response in these cells, we used DNA microarrays to compare IFN-induced transcription in IFN-sensitive SKOV3 cells, moderately resistant HT1080 cells, and HT1080 cells treated with U0126. We found that 267 genes were induced by IFN in SKOV3 cells, while only 98 genes were induced in HT1080 cells at the same time point. Furthermore, the expression of a distinct subset of IFN inducible genes, that included RIGI, GBP2, IFIT2, BTN3A3, MAP2, MMP7 and STAT2, was restored or increased in HT1080 cells when the cells were co-treated with U0126 and IFN. Bioinformatic analysis of the biological processes represented by these genes revealed increased representation of genes involved in the anti-viral response, regulation of apoptosis, cell differentiation and metabolism. Furthermore, introduction of constitutively active Ras into IFN sensitive SKOV3 cells reduced their IFN sensitivity and ability to activate IFN-induced transcription. This work demonstrates for the first time that activated Ras/MEK in human cancer cells induces downregulation of a specific subset of IFN-inducible genes. HT1080 cancer cells treated for 6 hours or 12 hours with interferon-alpha (500U/ml), the MEK inhibitor U0126 (20uM) or both, triplicate biological samples (18 samples). SKOV3 cells treated with interferon-alpha (500U/ml) for 6h, triplicate biological samples (6 samples).

2012-08-02 | E-GEOD-31019 | biostudies-arrayexpress

Bone marrow-derived macrophages express distinct transcriptional programs when activated by LPS, IFN-gamma and PAO.

Project description:mRNA microarray analysis of bone marrow derived macrophages treated under four conditions, including Naïve (N). Bone marrow derived macrophages (BMDM) were derived from the bone marrow of mice and cultured in the presence of PAO, IFN-gamma, or lipopolysaccharide (LPS). Profiled groups include Naive, LPS, IFN, PAO. Compared each of the groups (PAO, LPS, IFN) with Naïve group.

2013-08-08 | E-GEOD-48609 | biostudies-arrayexpress

IFN-b priming exacerbates LPS-driven proinflammatory cytokines in macrophages.

Project description:Purpose: We characterize the changes global expression profile in peripheral macrophages induced by LPS, IFN-b, and IFN-B+LPS treatment, using bulk RNA-sequencing. Methods: mRNA profiles of bulk macrophages obtained from WT mice following treatment with either saline, IFN-b, LPS, or IFN-b+LPS. Each treatment was performed in triplicate, and RNA-sequencing was performed on the Illumina 2500. Reads passing quality metric were aligned to the mm10 genome using annotations produced by ENSEMBL, and were analyzed at the transcript level using one-way ANOVA and fold change requirements. Results: We mapped approximately 20 million reads per sample to the mm10 genome, yielding 11385 reasonably-expressed transcripts. We identified 4372 transcripts with a p-value<0.05 and fold change>2 when compared between LPS v NS, IFNb v NS, and LPS+IFNb v NS. Of these, we identified 142 genes where priming by IFNb+LPS augmented the changes in expression induced by LPS or IFNb independently. This gene set indicated that IFNb exacerbates LPS_driven proinflammatory cytokin production. Conclusion: Here we show that IFNb priming sensitizes to TLD-driven inflammation through LPS stimulation.

2021-06-01 | GSE82087 | GEO

Microarray analysis of IFN-response

Project description:Type I interferon (IFN-α/β) is the first line of defense against viral infection. Mouse models have been pivotal to our understanding of IFN-α/β in immunity, although validation of these findings in humans has not been possible. We investigated a previously healthy child with fatal susceptibility to the live-attenuated measles, mumps and rubella (MMR) vaccine. By targeted resequencing we identified a homozygous mutation in the high-affinity interferon-α/β receptor (IFNAR2), which rendered cells unresponsive to IFN-α/β and led to unrestricted replication of IFN-attenuated viruses. Reconstitution of patient cells with wild-type IFNAR2 restored IFN-α/β responsiveness and viral resistance. Despite the failure to control vaccine viruses, the patient showed no evidence of susceptibility to conventional viral pathogens in vivo and adaptive immunity appeared normal. Human IFNAR2 deficiency therefore reveals an essential role for IFN-α/β in resistance to attenuated viruses, but significant and unexpected redundancy overall in antiviral immunity. Total RNA isolated from IFNAR2-deficient patient (in triplicate) and control (three independent control lines) fibroblasts treated with IFNalpha, IFNbeta or IFNgamma (1000 IU/mL) for 10h

2015-06-12 | E-GEOD-67737 | biostudies-arrayexpress

TCL001: Calu-3 cells treated with either IFN alpha or gamma

Project description:Purpose of experiment was to compare transcriptomics of Calu-3 cells treated with either INF alpha or gamma. Calu-3 cells were treated with 1000 Units/ml of INFa (Sigma I4276) or 500 Units/ml of IFN γ (Sigma I3265). Cells were collected for RNA isolation at 0, 3, 6, and 18 or 22 h post treatment. Each treated sample was done in triplicate. (Triplicates are defined as 3 different wells, plated at the same time using the same cell stock for all replicates.)There are triplicate time-matched mock for each time point from the same cell stock as rest of samples. The NIAID Systems Virology Center

2011-11-01 | E-GEOD-33264 | biostudies-arrayexpress

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