Global CpG methylation analysis of primary endothelial cells before and after TNFa stimulation
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ABSTRACT:
PROVIDER: PRJNA604987 | ENA |
REPOSITORIES: ENA
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Project description:Endothelial cells are a primary site of leukocyte recruitment during inflammation. An increase in tumor necrosis factor-alpha (TNFa) levels as a result of infection or some autoimmune diseases can trigger this process. Several autoimmune diseases are now treated with TNFa inhibitors. However, genomic alterations that occur as a result of TNF-mediated inflammation are not well understood. To investigate molecular targets and networks resulting from increased TNFa, we measured DNA methylation and gene expression in 40 human umbilical vein endothelial cell primary cell lines before and 24 hours after stimulation with TNFa via microarray.
2020-02-06 | GSE144804 | GEO
Project description:Endothelial cells are a primary site of leukocyte recruitment during inflammation. An increase in tumor necrosis factor-alpha (TNFa) levels as a result of infection or some autoimmune diseases can trigger this process. Several autoimmune diseases are now treated with TNFa inhibitors. However, genomic alterations that occur as a result of TNF-mediated inflammation are not well understood. To investigate molecular targets and networks resulting from increased TNFa, we measured DNA methylation and gene expression in 40 human umbilical vein endothelial cell primary cell lines before and 24 hours after stimulation with TNFa via microarray.
2020-02-06 | GSE144803 | GEO
Project description:Global expression analysis of primary endothelial cells before and after TNFa stimulation
| PRJNA604979 | ENA
Project description:Analysis of primary endothelial cells before and after TNFa stimulation
| PRJNA604981 | ENA
Project description:Endothelial cells are a primary site of leukocyte recruitment during inflammation. An increase in tumor necrosis factor-alpha (TNFa) levels as a result of infection or some autoimmune diseases can trigger this process. Several autoimmune diseases are now treated with TNFa inhibitors. However, genomic alterations that occur as a result of TNF-mediated inflammation are not well understood. To investigate molecular targets and networks resulting from increased TNFa, we measured DNA methylation and gene expression in 40 human umbilical vein endothelial cell primary cell lines before and 24 hours after stimulation with TNFa via microarray. Weighted gene co-expression network analysis identified 15 gene groups (modules) with similar expression correlation patterns; four modules showed a strong association with TNFa treatment. Genes in the top TNFa-associated module were all up-regulated, had the highest proportion of hypomethylated regions, and were associated with 136 Disease Ontology terms, including autoimmune/inflammatory, infectious and cardiovascular diseases, and cancers. They included chemokines CXCL1, CXCL10 and CXCL8, and genes associated with autoimmune diseases including HLA-C, DDX58, IL4, NFKBIA and TNFAIP3. Cardiovascular and metabolic disease genes, including APOC1, ACLY, ELOVL6, FASN and SCD, were overrepresented in a module that was not associated with TNFa treatment. Of 223 hypomethylated regions identified, several were in promoters of autoimmune disease GWAS loci (ARID5B, CD69, HDAC9, IL7R, TNIP1 and TRAF1). Results reveal specific gene groups acting in concert in endothelial cells, delineate those driven by TNFa, and establish their relationship to DNA methylation changes, which has strong implications for understanding disease etiology and precision medicine approaches.
| S-EPMC7108734 | biostudies-literature
Project description:Kidney organoids are a valuable and innovative model to understand genetic diseases, kidney development and transcriptomic dynamics. However, their proteome has not been analyzed so far. Here, we analyzed the organoid proteome after treatment of organoids with 5ng/mL TNFalpha for 24h and 48h compared with vehicle control (VC). Incubation of organoids (day 25 of differentiation) with TNFalpha led to an activation of NFkappaB signaling, and, interestingly, secretion of cytokines and complement components, alongside with extracellular matrix components. Interestingly, this signaling system directly links inflammatory signaling, production of cytokines and complement; and production of extracellular matrix. Thus, we provide a repository of kidney organoid proteins that revealed the potential to model pathophysiological pathways beyond genetic diseases. Organoids were grown according to the Freedman protocol (Freedman, Brooks et al. 2015, Czerniecki, Cruz et al. 2018). The IPSCs were differentiated for a three-week period until first spheroids from. We started TNFa stimulation at day 25, with the 24h stimulation ending on day 26 and the 48h stimulation ending on day 27. We chose day 25 because it lies centrally in the day 21 to day 29 window, where we observe reproducible spheroids with limited off-target differentiation of organoids, which becomes an issue after day 29.
2023-05-12 | PXD029718 | Pride
Project description:Kidney organoids are a valuable and innovative model to understand genetic diseases, kidney development and transcriptomic dynamics. However, their proteome has not been analyzed so far. Here, we analyzed the organoid proteome after treatment of organoids with 5ng/mL TNFalpha for 24h and 48h compared with vehicle control (VC). Incubation of organoids (day 25 of differentiation) with TNFalpha led to an activation of NFkappaB signaling, and, interestingly, secretion of cytokines and complement components, alongside with extracellular matrix components. Interestingly, this signaling system directly links inflammatory signaling, production of cytokines and complement; and production of extracellular matrix. Thus, we provide a repository of kidney organoid proteins that revealed the potential to model pathophysiological pathways beyond genetic diseases. Organoids were grown according to the Freedman protocol (Freedman, Brooks et al. 2015, Czerniecki, Cruz et al. 2018). The IPSCs were differentiated for a three-week period until first spheroids from. We started TNFa stimulation at day 25, with the 24h stimulation ending on day 26 and the 48h stimulation ending on day 27. We chose day 25 because it lies centrally in the day 21 to day 29 window, where we observe reproducible spheroids with limited off-target differentiation of organoids, which becomes an issue after day 29.
2023-05-12 | PXD029696 | Pride
Project description:XIAP (X chromosome-linked inhibitor of apoptosis; ILP, BIRC4) is involved not only in apoptosis, but also in signal tranduction in the NF-kappaB, TGF-beta, bone morphogenic protein, and JNK signalling pathways. We have analyzed whether XIAP deletion leads to changes in gene expression, particularly after inflammatory stimulation. Experiment Overall Design: Fibroblasts from wild-type and XIAP knockout mice were analyzed with and without TNFa stimulation (4 hours) using Affymetrix U74Av2 arrays.
2008-11-15 | E-GEOD-3700 | biostudies-arrayexpress
Project description:To understand the transcripts induced by TNFa and how these may interact in inflammatory networks, the transcriptome of HUCECs stimulated with TNFa was examined in 3 different pools each cosisting of 10 different HUVEC isolates. In the study present here, HUVEC isolates from 3 pools of 10 different individuals were cultured until passage 4 in fully supplemented growth conditions. Passage 4 HUVEC isolates were then treated with TNFa (10ng/ml), with RNA extracted at time points 0, 1, 1.5, 2, 4, 5, and 6hrs after TNFa treatment . RNA was extracted and hybridised onto CodeLink microarrays.
2011-11-29 | E-GEOD-27870 | biostudies-arrayexpress
Project description:To understand the transcripts induced by TNFa and how these may interact in inflammatory networks, the transcriptome of HUCECs stimulated with TNFa was examined in 3 different pools each cosisting of 10 different HUVEC isolates.
2011-11-29 | GSE27870 | GEO