Three human cell types respond to multi-walled carbon nanotubes and titanium dioxide nanobelts with cell-specific transcriptomic and proteomic expression
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
SUBMITTER: Susan Tilton
PROVIDER: E-GEOD-42069 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:To identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics. Transcriptional responses were measured by global microarray analysis of cells in culture. Groups (N=3 biological replicates) of Caco-2/HT29-MTX cells exposed to 0, 10 or 100 ug/ml MWCNT or TiO2-NB nanoparticles for 1 or 24 hr.
2012-12-15 | E-GEOD-42066 | biostudies-arrayexpress
Project description:To identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics. Transcriptional responses were measured by global microarray analysis of cells in culture. Groups (N=3 biological replicates) of SAE cells exposed to 0, 10 or 100 ug/ml MWCNT or TiO2-NB nanoparticles for 1 or 24 hr.
2012-12-15 | E-GEOD-42067 | biostudies-arrayexpress
Project description:To identify key biological pathways that define toxicity or biocompatibility after nanoparticle exposure, three human cell types were exposed in vitro to two high aspect ratio nanoparticles for 1 hr or 24 hr and collected for global transcriptomics. Transcriptional responses were measured by global microarray analysis of cells in culture. Groups (N=3 biological replicates) of THP-1 cells exposed to 0, 10 or 100 ug/ml MWCNT or TiO2-NB nanoparticles for 1 or 24 hr.
2012-12-15 | E-GEOD-42068 | biostudies-arrayexpress
Project description:To assess the effect of carbon nanotubes substrated on dendritic cell (DCs) properties, DCs were generated from human monocytes of healthy donors as previously described (Aldinucci A et al, 2010). In particular, isolated monocytes were cultured for 6 days in medium supplemented with GM-CSF (1000U/ml) and IL-4 (1000U/ml), in presence or absence of multi-walled carbon nanotubes (MWCNT); then DCs were activated by 24 hours of incubation with LPS (1ug/ml). RNA extracted from floating and CNT adherent DCs were then used for transcriptional profilingthen used
2015-04-01 | E-MEXP-3560 | biostudies-arrayexpress
Project description:Our previous proteomics analysis suggested down-regulation of mitochondrial aconitase (ACO2) plays an important role in colorectal cancer. To evaluate the effect of mitochondrial aconitase overexpression on the metabolic and signaling pathway changes in colon cancer cell line HT29, we generated two ACO2 overexpressing cell lines #C and #UD and the mock-transfected vector control #VE. HT29 colon cancer cells overexpressing ACO2 exhibited lower rate of cell proliferation in vitro and reduced tumor growth potential in nude mice. In order to understand the signaling pathway changes, cDNA microarray analysis using GeneChips from Affymetrix were carried out.
2010-01-14 | E-MEXP-1996 | biostudies-arrayexpress
Project description:Background. Rheumatoid arthritis (RA) is a chronic inflammatory and destructive joint disease, characterized by overexpression of pro-inflammatory/-destructive genes and other activating genes (e.g., proto-oncogenes) in the synovial membrane (SM). The gene expression in disease is often characterized by significant inter-individual variances via specific synchronization/ desynchronization of gene expression. To elucidate the contribution of the variance to the pathogenesis of disease, expression variances were tested in SM samples of RA patients, osteoarthritis (OA) patients, and normal controls (NC). Results. For the comparison between RA and NC, 568 genes with significantly different variances in the 2 groups (p < 0.05; Bonferroni/Holm corrected Brown-Forsythe version of the Levene-Test) were selected. For the comparison between RA and OA, 333 genes were selected. Using the Kyoto encyclopedia of genes and genomes (KEGG), 10 pathways/complexes significantly affected by higher gene expression variances were identified in RA compared to NC, including cytokine â cytokine receptor interactions, the TGF-pathway, and anti-apoptosis. Compared to OA, 3 pathways with significantly higher variances were identified in RA (e.g., B cell receptor signaling, VEGF signaling). Functionally, the majority of the identified pathways is involved in the regulation of inflammation, proliferation, cell survival, and angiogenesis. Conclusion. In RA, a number of disease-relevant or even disease-specific pathways/complexes are characterized by broad intra-group, inter-individual expression variances. This indicates that RA pathogenesis in different individuals may depend to a lesser extent on common alterations of the expression of specific key genes, but on individual-specific alterations of different genes resulting in common disturbances of key pathways. Experiment Overall Design: Expression variances were tested in synovial membrane samples of rheumatoid arthritis patients, osteoarthritis patients, and normal controls (see publication for further details).
2008-10-25 | E-GEOD-12021 | biostudies-arrayexpress
Project description:HT29 cells was infected with EV71 at MOI 1 or nil respectively and harvested at 36hpi We use miRNA microarray to profile and identify miRNA which are up or down regulated due to EV71 infection 3 biological replicate (6 samples)
2014-05-08 | E-GEOD-57372 | biostudies-arrayexpress
Project description:Discrimination of rheumatoid arthritis (RA) patients from patients with other inflammatory/degenerative joint diseases or healthy individuals purely on the basis of genes differentially expressed in high-throughput data has proven very difficult. Thus, the present study sought to achieve such discrimination by employing a novel unbiased approach using rule-based classifiers. Three multi-center genome-wide transcriptomic data sets (Affymetrix HG- U133 A/B) from a total of 79 individuals, including 20 healthy controls (control group - CG), as well as 26 osteoarthritis (OA) and 33 RA patients, were used to infer rule- based classifiers to discriminate the disease groups. The rules were ranked with respect to Kiendl’s statistical relevance index, and the resulting rule set was optimized by pruning. The rule sets were inferred separately from data of one of three centers and applied to the two remaining centers for validation. All rules from the optimized rule sets of all centers were used to analyze their biological relevance applying the software Pathway Studio. The optimized rule sets for the three centers contained a total of 29, 20, and 8 rules (including 10, 8, and 4 rules for ‘RA’), respectively. The mean sensitivity for the prediction of RA based on six center-to-center tests was 96% (range 90% to 100%), that for OA 86% (range 40% to 100%). The mean specificity for RA prediction was 94% (range 80% to 100%), that for OA 96% (range 83.3% to 100%). The average overall accuracy of the three different rule-based classifiers was 91% (range 80% to 100%). Unbiased analyses by Pathway Studio of the gene sets obtained by discrimination of RA from OA and CG with rule-based classifiers resulted in the identification of the pathogenetically and/or therapeutically relevant interferon-gamma and GM-CSF pathways. First-time application of rule-based classifiers for the discrimination of RA resulted in high performance, with means for all assessment parameters close to or higher than 90%. In addition, this unbiased, new approach resulted in the identification not only of pathways known to be critical to RA, but also of novel molecules such as serine/threonine kinase 10. Three multi-center genome-wide transcriptomic data sets (Affymetrix HG- U133 A/B) from a total of 79 individuals, including 20 healthy controls (control group - CG), as well as 26 osteoarthritis (OA) and 33 RA patients, were used to infer rule- based classifiers to discriminate the disease groups. The rules were ranked with respect to Kiendl’s statistical relevance index, and the resulting rule set was optimized by pruning. The rule sets were inferred separately from data of one of three centers and applied to the two remaining centers for validation. All rules from the optimized rule sets of all centers were used to analyze their biological relevance applying the software Pathway Studio.
2014-03-05 | E-GEOD-55584 | biostudies-arrayexpress
Project description:TF antigen specific Sclerotium rolfsii lectin (SRL) induces apoptosis in human colon cancer HT29 cells and has tumour suppressing effect in vivo as reported earlier. In this study, we investigated the signaling pathways to identify the signature genes that lead to apoptosis of HT29 cells by mRNA and miRNA microarray analysis. HT29 cells were treated with SRL (20 ug/ml) for 2, 4, 8 12, 24 and 48h and gene expression microarray analysis was performed using SurePrint G3 Human Gene Expression Microarray kit. Several hundred entities were differentially regulated with a fold change value of greater than or equal to 2 and p value less than or equal to 0.05 following interaction of SRL at all-time points. Pathway analysis using GeneSpring 12.6.1 revealed that the MAPK signaling pathway is affected as early as 2h while cell cycle, DNA replication and apoptosis pathways are most significantly affected at 24 and 48h. SRL induced immediate over-expression of the transcription factor c-Jun as early as 2h. Very few miRNAs were found to be differentially regulated at 2 and 4h, however, a significant change in differentially expressed miRNAs were noticed at 12h with the miRNA gene target list significantly overlapping with the differential gene expression. The study suggests that the interaction of SRL with HT29 cells triggers apoptosis by affecting cell cycle, DNA replication and apoptosis signaling pathways. The observed effects may be initiated by affecting MAP kinase pathway and mediated by c-JUN. These findings were further validated by qRT-PCR and western blotting. The findings will enable to exploit and develop SRL as a possible targeted drug for cancer therapeutics.
2014-10-14 | E-MTAB-3003 | biostudies-arrayexpress
Project description:Ror gamma t-deficient mice lack group 3 Innate Lymphoid Cells (ILC3s) and as a result have increased tissue damage and diminished tissue repair in response to insult. To identify repair programs associated with ILC3 presence the transcriptomes of small intestinal stem cells exposed to damage in the presence or absence of ILC3 were compared. Small intestinal damage was induced in Ror gamma t-deficient Lgr5 reporter mice and littermate controls. Small intestinal epithelial stem cells were purified at days 1 and 4 after damage and subjected to RNA sequencing.
2018-06-29 | E-MTAB-6639 | biostudies-arrayexpress