RNAseq analysis in TNF treated HUVEC cells compared to controls
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Illumina Genome Analyzer II
ORGANISM(S): Homo sapiens
SUBMITTER: Martin McBride W
PROVIDER: E-MTAB-8299 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To understand the transcripts regulated by inflammation and how this regulation may differ between different individuals, the transcriptome of HUVECs stimulated with inflammatory mediators was examined in 9 different individuals. In the study present here, HUVEC isolates from 9 different individuals were cultured until passage 4 in fully supplemented growth conditions. Passage 4 HUVEC isolates were then treated with a cocktail of inflammatory mediators (10ng/ml TNF-α, Il-1β, Il-8) for a period of 24 hours prior to RNA extraction. RNA was extracted and hybridised onto CodeLink microarrays. The expression profiles in the inflammatory mediator treated condition were examined along side a superset of the same biological replicates that were untreated (also submitted), to facilitate assessment of the resting transcriptome.
2011-07-19 | E-GEOD-23069 | biostudies-arrayexpress
Project description:Human umbilical vein endothelial cells (HUVEC) were isolated from umbilical cords from four different donors, as previously described (Cooke et al., 1993). Cells were maintained in Medium 199 (M199, Invitrogen) containing 20% fetal calf serum, 28g/ml gentamycin, 2.5g/ml amphotericin B, 1ng/ml epidermal growth factor and 1g/ml hydrocortisone (all from Sigma) for 48 hours prior to processing. HUVEC cultures isolated using this method were 96-98% pure, determined by positive staining by flow cytometry of CD105, CD31 and vWF and the expression of elevated levels of intracellular adhesion molecule (ICAM-1) and E-selectin following stimulation with the inflammatory cytokine interleukin-1. Total HUVEC RNA was isolated using the RNeasy mini kit with QIAshredder (Qiagen) according to the manufacturers instructions. RNA integrity number was >8.0 for all samples.
2016-09-30 | E-MTAB-4897 | biostudies-arrayexpress
Project description:In this study, we established a rat small intestinal cell (IEC-6) injury model with tumor necrosis factor-α (TNF-α). Then, we added the exosomes from TNF- α damaged IEC-6 (TNF-α-exo), co-cultured with BMMSCs exosomes (BM-exo) and heme oxygenase-1 modified BMMSCs (HBM-exo) system exosomes into IEC-6 cells injured by TNF- α inflammation. After 48 hours, IEC-6 cells were collected for proteomic detection.
2020-06-29 | PXD017002 | Pride
Project description:To assess if HUVEC and HUAEC differ in suscptibility to inflammation and inflammation resolution, the cells were stimulated for 24 hrs with TNF followed by RNA isolation. Two additional groups were first stimulated with TNF (24 hr) followed by TNF removal (12 and 24 hrs). Expression profiles were compared to basal conditions, i.e. cells cultured in normal medium We used micro-arrays to assess if Gene-xpression profiles between HUVEC and HUAEC differ under inflammatory conditions and under conditions of inflammation resolution
2023-10-04 | GSE179478 | GEO
Project description:Mitochondrial oxidative phosphorylation (OXPHOS) fuels cellular ATP demands. OXPHOS defects lead to severe human disorders with unexplained tissue specific pathologies. Mitochondrial gene expression is essential for OXPHOS biogenesis since core subunits of the complexes are mitochondrial-encoded. COX14 is required for translation of COX1, the central mitochondrial-encoded subunit of complex IV. Here we generated a COX14 mouse mutant corresponding to a patient with complex IV deficiency. COX14M19I mice display broad tissue-specific pathologies. A hallmark phenotype is severe liver inflammation linked to release of mitochondrial RNA into the cytosol sensed by RIG-1 pathway. We find that mitochondrial RNA release is triggered by increased reactive oxygen species production in the absence of complex IV. Additionally, we also generated a COA3Y72C mouse, affected in COX1 biogenesis, which displays a similar yet milder inflammatory phenotype. Our study provides mechanistic insight into how defective mitochondrial gene expression causes tissue-specific inflammation.
2024-07-25 | PXD041783 | Pride
Project description:Human retinal pigment epithelial (HRPE) cells in culture respond to inflammatory cytokines (IFN-? + TNF-? + IL-1? ) by increasing the expression of many cytokines and chemokines. The goal of this study was to delineate the role of miRNA in this process. We employed microarray analysis to study the effect of inflammatory cytokines on the miRNA expression in HRPE cells. HRPE cells were treated with a mixture of IFN-? (100 u), TNF-? (10 ng/ml) and IL-1? (10 ng/ml) for 16 hours, and the miRNA expression was analyzed using RNA preparations isolated from control and treated cells. The experiment was repeated. Control samples were labeled with Cy3 while the treated samples with Cy5.
2010-11-11 | E-GEOD-23979 | biostudies-arrayexpress
Project description:Membrane ion channels of the calcium homeostasis modulator (CALHM) family promote cell-cell crosstalk at synapses via ATP release, where ATP acts as a neurotransmitter. CALHM6, the only CALHM highly expressed in immune cells, has been linked to induction of natural killer (NK) cell anti-tumour activity. Its mechanism of action and broader functions in the immune system are, however, unclear. Here we generated Calhm6-/- mice and report that CALHM6 is important for regulating the early innate control of Listeria monocytogenes infection in vivo. We find that CALHM6 is upregulated in macrophages by pathogen-derived signals, and that it relocates from intracellular compartment to the macrophage-NK cell synapse, facilitating ATP release and controlling the kinetics of NK cell activation. Anti-inflammatory cytokines terminate CALHM6 expression. CALHM6 forms an ion channel when expressed in the plasma membrane of Xenopus oocytes, where channel opening is controlled by a conserved acidic residue, E119, but CALHM6 is localized to intracellular compartments in mammalian cells. Our results contribute to understanding of neurotransmitter-like signal exchange between immune cells that fine-tunes the timing of innate immune responses.
2023-02-01 | GSE223008 | GEO
Project description:In the hematopoietic microenvironment, endothelial cells (ECs) play an important role in the regulation of hematopoietic cell proliferation and trafficking. We previously demonstrated that EC stimulated with tumor necrosis factor alpha (TNF-α) induce the generation of dendritic cells from CD34(+) stem cells, whereas in contrast, interleukins were capable of inducing the proliferation of hematopoietic and myeloid progenitors. In order to identify potentially new soluble factors which greatly impact the self-renewal, proliferation and differentiation of CD34+ hematopoietic stem cells (HSC), we examined the expression profiles of IL-1ß, IL-3 and IL-6 stimulated human umbilical vein endothelial cells (HUVEC).
2011-07-01 | GSE22325 | GEO
Project description:Aspergillus fumigatus is an angioinvasive fungal pathogen and the main etiologic agent causing invasive aspergillosis. Upon contact with human umbilical vein endothelial cells (HUVECs), this fungus induces cellular injury, inflammatory response and a pro-thrombotic phenotype. The pathogen molecules involved in this processes are however still unknown. A. fumigatus hyphae have been shown to produce, both in vivo and in vitro, an extracellular matrix composed of galactomannan, galactosaminogalactan and α-(1,3)-glucan. The deletion of the UDP-Galp mutase results in a mutant with a very sticky phenotype, due to the increase in the galactosaminogalactan content in the cell surface. The overexpression of galactosaminogalactan in this mutant was confirmed by immunofluorescence microscopy with a monoclonal antibody. Interestingly, the adhesion of ∆ugm1 germlings to HUVECs was significantly higher in comparison to the wild type strain. The ∆ugm1 adhesion capacity was followed by an increment in the cytokine secretion and tissue factor expression by infected endothelial cells. Using a shotgun proteomic approach with label-free quantification, we were able to search and compare pathways regulated in endothelial cells challenged with A. fumigatus, wild type and ∆ugm1. The deletion of the UGM1 gene in A. fumigatus induced changes in the endothelial cell response, maily related to immune and stress responses. In addition, the purified urea soluble fraction of galactosaminogalactan was able to induce TNF-α secretion by HUVECs and also regulate coincident pathways identified in the mutant interaction condition. This work describes for the first time the impact of the modifications of the hyphal surface galactosaminogalactan on the endothelial cell responses to A. fumigatus.
2016-06-22 | PXD002823 | Pride
Project description:Carbon monoxide (CO) abrogates TNF-alpha mediated inflammatory responses in endothelial cells, yet, the underlying mechanism hereof is still elusive. We sought to explore potential mechanisms by which CO down-regulates VCAM-1 expression on TNF-alpha stimulated human umbilical vein endothelial cells (HUVEC). By genome-wide gene expression profiling and pathway analysis we studied the relevance of particular pathways for the anti-inflammatory effect of CO. In CO-releasing molecules-3 (CORM-3) stimulated HUVEC, significant changes in gene expression were found for genes implicated in the proteasome and porphyrine pathways. Although proteasome activities were increased by CORM-3, proteasome inhibitors did not abolish CORM-3‘s effect. Likewise, HO-1 inhibitors did not abrogate the ability of CORM-3 to down-regulate VCAM-1 expression. MAPK p38 was inhibited by CORM-3. Accordingly, VCAM-1 expression was down-regulated by the p38 inhibitor SB203580. Down-regulation of VCAM-1 by CORM-3 only occurred at concentrations that partly inhibit ATP production. Sodium azide and oligomycin paralleled the effect of CORM-3 in this regard. In conclusion, down-regulation of VCAM-1 by CORM-3 seems to be mediated via inhibition of p38 and mitochondrial respiration. Although CORM-3 up-regulates several genes in the ubiquitin proteasome sytem (UPS) or porphyrin pathway, there is no evidence that these changes are involved in the anti-inflammatory properties of CORM-3. In this study we focused on the potential of CORM-3 to downregulate the expression of TNF-alpha mediated inflammataroy genes
2011-07-11 | E-GEOD-22175 | biostudies-arrayexpress