The 14-week experiment included three groups: 1) the Acute Cpn group, with one C. pneumoniae inoculation at the age of 9 wks; 2) the Chronic Cpn group, with three C. pneumoniae inoculations at the age of 9, 11, and 13 wks; and 3) the control group, with three SPG inoculations at the age of 9, 11, and 13 wks. The mice were sacrificed at the age of 14 wks. The 24-week experiment included four groups: 1) the recurrent A. actinomycetemcomitans infection group, with ten A. actinomycetemcomitans inoculations once a week from the age of 14 to 23 wks; 2) the chronic C. pneumoniae infection group, with three C. pneumoniae inoculations at the age of 9, 11, and 13 wks; 3) the combined chronic C. pneumoniae and recurrent A. actinomycetemcomitans infection group, with three C. pneumoniae inoculations at the age of 9, 11, and 13 wks, and ten A. actinomycetemcomitans inoculations once a week from the age of 14 to 23 wks; and 4) the control group, with three SPG inoculations at the age of 9, 11, and 13 wks, and ten 0.9% NaCl inoculations once a week from the age of 14 to 23 wks. The mice were sacrificed at the age of 24 wks.Epididymal and inguinal AT gene expression was analyzed using an Illumina Mouse WG-6 v2.0 platform.
The effect of proatherogenic pathogens on adipose tissue transcriptome and fatty acid distribution in apolipoprotein E-deficient mice.
Sex, Age, Specimen part
View SamplesPpargc1a overexpression in heart tissue measured using RNA sequencing Overall design: RNA expression profiles were generated using RNA-seq from control (N=3) and Ppargc1a overexpressing (N=3) mice
Peroxisome proliferator-activated receptor-γ coactivator 1 α1 induces a cardiac excitation-contraction coupling phenotype without metabolic remodelling.
Specimen part, Treatment, Subject
View SamplesWe show that Bmx-deficiency reduces angiotensin II -induced cardiac hypertrophy and pathological gene expression
Endothelial Bmx tyrosine kinase activity is essential for myocardial hypertrophy and remodeling.
Sex
View SamplesStudy of gene expression patterns of Drosophila melanogaster Sesb1 mutants compared to wild type
Phenotypic rescue of a Drosophila model of mitochondrial ANT1 disease.
Sex
View SamplesThe aim of this dataset was to study in detail the transcription kinetics initiated by cytokines IL-12 and IL-4 in early differentiation of Th1 and Th2 cells, respectively.
An integrative computational systems biology approach identifies differentially regulated dynamic transcriptome signatures which drive the initiation of human T helper cell differentiation.
Specimen part
View SamplesRecognition and response to gram-positive bacteria by macrophages and dendritic cells is mediated in part through TLR2. We found that that Streptococcus pneumoniae cell wall fragments, containing primarily peptidoglycan and teichoic acids, induced prodigious secretion of IL-10 from macrophages and dendritic cells and was dependent on TLR2 and NOD2, a cytoplasmic CARD-NACHT-LRR protein encoded by Card15. IL-10 secretion in response to cell walls was also dependent on RICK/RIP2, a kinase associated with NOD2, and MYD88 but independent of the ERK/p38 pathway. The reduction of IL-10 secretion by cell wall-activated NOD2-deficient myeloidderived cells translated into downstream effects on IL-10 target gene expression and elevations in subsets of pro-inflammatory cytokine expression normally restrained by autocrine/paracrine effects of IL-10. Since NOD2 is linked to aberrant immune responses in Crohns Disease patients bearing mutations in CARD15, the temporal and quantitative effects of the TLR2/NOD/RICK pathway on IL-10 secretion may affect homeostatic control of immune responses to gram-positive bacteria.
The TLR2-MyD88-NOD2-RIPK2 signalling axis regulates a balanced pro-inflammatory and IL-10-mediated anti-inflammatory cytokine response to Gram-positive cell walls.
No sample metadata fields
View SamplesSpecial AT-rich binding protein 1 (SATB1) is a global chromatin organizer and a transcription factor induced by interleukin-4 (IL-4) during the early T helper 2 (Th2) cell differentiation. In this study, we investigated the role of SATB1 in T helper cell differentiation by performing gene expression profiling of human differentiating Th cells in which expression of SATB1 was downregulated by RNA interference (RNAi). Our results indicate that SATB1 is involved in the regulation of more than three hundred genes in primary human CD4+ T cells, including several IL-12 and/or IL-4 regulated factors, suggesting a role in the development or function of Th subtypes.
SATB1 dictates expression of multiple genes including IL-5 involved in human T helper cell differentiation.
No sample metadata fields
View SamplesThe study aims at identifying transcriptional changes induced by in vitro polarization of human cord blood CD4+ cells towards Th17 subtype with combination of IL6, IL1b and TGFb by using timeseries data.
Identification of early gene expression changes during human Th17 cell differentiation.
Specimen part, Time
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene expression profiling of immune-competent human cells exposed to engineered zinc oxide or titanium dioxide nanoparticles.
Specimen part, Treatment, Time
View SamplesA comprehensive in vitro assessment of two commercial metal oxide nanoparticles, TiO2 and ZnO, was performed using human monocyte-derived macrophages (HMDM), monocyte-derived dendritic cells (MDDC), and T cell leukemia-derived cell line (Jurkat). TiO2 nanoparticles were found to be non-toxic whereas ZnO nanoparticles caused dose-dependent cell death. Subsequently, global gene expression profiling was performed to identify signaling pathways underlying the cytotoxicity caused by ZnO nanoparticles. Analysis was done with doses, 1g/ml and 10g/ml after 6 and 24 hours of exposure. Interestingly, 2703 genes were significantly differentially expressed in HMDM upon exposure to 10g/ml ZnO nanoparticles, while in MDDCs only 12 genes were affected. In Jurkat cells, 980 genes were differentially expressed. It is noteworthy that the gene expression of metallothioneins was upregulated in all the three cell types. In addition to the common ZnO-inducible changes, a notable proportion of the genes were regulated in a cell type-specific manner. Using a panel of ZnO nanoparticles, we obtained an additional support that the cellular response to ZnO nanoparticles is caused by particle dissolution. Gene ontology analysis revealed that the top biological processes disturbed in HMDM and Jurkat cells were regulating cell death and growth. In addition, genes controlling immune system development were affected. Bioinformatics assessment showed that the top human disease category associated with ZnO-responsive genes in both HMDM and Jurkat cells was cancer. Overall, the study revealed novel genes and pathways for mediating ZnO nanoparticle-induced toxicity and demonstrated the value of assessing nanoparticle responses through combined transcriptomics and bioinformatics approach.
Gene expression profiling of immune-competent human cells exposed to engineered zinc oxide or titanium dioxide nanoparticles.
Specimen part, Treatment, Time
View Samples