Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

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-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.

ORGANISM(S): Homo sapiens

SUBMITTER: Johanna Hol

PROVIDER: E-GEOD-37624 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Interleukin-33 drives a proinflammatory endothelial activation that selectively targets nonquiescent cells.

Pollheimer Jürgen J Bodin Johanna J Sundnes Olav O Edelmann Reidunn J RJ Skånland Sigrid S SS Sponheim Jon J Brox Mari Johanna MJ Sundlisaeter Eirik E Loos Tamara T Vatn Morten M Kasprzycka Monika M Wang Junbai J Küchler Axel M AM Taskén Kjetil K Haraldsen Guttorm G Hol Johanna J

Arteriosclerosis, thrombosis, and vascular biology 20121115 2

<h4>Objective</h4>Interleukin (IL)-33 is a nuclear protein that is released from stressed or damaged cells to act as an alarmin. We investigated the effects of IL-33 on endothelial cells, using the prototype IL-1 family member, IL-1β, as a reference.<h4>Methods and results</h4>Human umbilical vein endothelial cells were stimulated with IL-33 or IL-1β, showing highly similar phosphorylation of signaling molecules, induction of adhesion molecules, and transcription profiles. However, intradermally ...[more]

PMID: 23162017

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Project description:In colorectal cancer, increased expression of the CXC chemokine receptor 4 (CXCR4) has been shown to provoke metastatic disease due to the interaction with its ligand stromal cell-derived factor 1 (SDF-1). Recently, a second SDF-1 receptor, CXCR7, was found to enhance tumor growth in solid tumors. Albeit signaling cascades via SDF-1/CXCR4 have been intensively studied, the significance of the SDF-1/CXCR7-induced intracellular communication triggering malignancy is still only marginally understood. In tumor tissue of 52 colorectal cancer (CRC) patients, we observed that expression of CXCR7 and CXCR4 increased with tumor stage, tumor size, and lymph node infiltration. Asking whether activation of CXCR4 or CXCR7 might result in a similar expression pattern, we performed microarray expression analyses using lentivirally CXCR4- and/or CXCR7-overexpressing SW480 colon cancer cell lines with and without stimulation by SDF-1M-NM-1. Gene regulation via SDF-1M-NM-1/CXCR4 and SDF-1M-NM-1/CXCR7 was completely different and partly antidromic. Expressions of the differentially expressed genes AKR1C3, AXL, EGFR, IGFBP7, IL24, TNNC1, TRIP6 were confirmed by qPCR. Differentially regulated genes were assigned by GO to migration and lipid metabolic processes. Furthermore, using the in silico gene set enrichment analysis we showed for the first time that expressions of miR-217 and miR-218 were increased in CXCR4 and reduced in CXCR7 cells after stimulation with SDF-1M-NM-1. As expected, their putative target mRNAs were inversely expressed. Functional assays exerted that exposure to SDF-1M-NM-1 resulted in strongly amplified invasiveness and chemosensitivity of CXCR4-expressing cells. CXCR7 overexpression led to reduced invasiveness which could only be marginally increased by SDF-1M-NM-1. The CXCR4 antagonist plerixafor significantly reduced invasiveness of CXCR4-overexpressing cells only. Similarly, compared to control cells, CXCR4 cells showed increased sensitivity against 5-FU, while CXCR7 cells were more chemoresistant. These opposing results for CXCR4- or CXCR7-overexpressing colon carcinoma cells demand an unexpected attention in the clinical application of chemokine receptor antagonists like Plerixafor. 24 samples

Dataset Information

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

Publications

Interleukin-33 drives a proinflammatory endothelial activation that selectively targets nonquiescent cells.

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