The experiment consists of 31 Systemic Lupus Erythematosus patient blood samples and 29 healthy donor blood samples. Overall design: Whole blood was collected in PaxGene tubes from 31 SLE and 29 healthy donors.
Machine learning applied to whole-blood RNA-sequencing data uncovers distinct subsets of patients with systemic lupus erythematosus.
Sex, Age, Specimen part, Subject
View SamplesLearn about the transcriptome profiling of zona glomerulosa (ZG), zona fasciculata (ZF) and aldosterone-producing adenomas (APA) in human adrenals
DACH1, a zona glomerulosa selective gene in the human adrenal, activates transforming growth factor-β signaling and suppresses aldosterone secretion.
Specimen part, Disease
View SamplesAffymetrix U133A comparison of two groups (10 samples each): untreated (androgen-dependent) primary prostate cancer (Gleasons 5-9) and androgen-independent primary prostate cancer. All samples were microdissected for tumor cells only.
Molecular alterations in primary prostate cancer after androgen ablation therapy.
No sample metadata fields
View SamplesThis SuperSeries is composed of the SubSeries listed below.
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line, Treatment
View SamplesWe used the microarray analysis to detail the gene expression profile from the leukemic cell line HL-60
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line
View SamplesIdentification of the all RNA species associated with DNMT1. Using a comparative genome-scale approach we identified and correlated the RNA species physically associated with DNMT1 and proximal to the annotated genes to the methylation status of the corresponding loci and expression levels of the respective genes. This comparative approach delineated the first -DNMT1 centered- 'epitranscriptome' map, a comprehensive map cross-referencing DNMT1-interacting transcripts to (i) DNA methylation and (ii) gene expression profile. Overall design: Relationship between DNMT1-RNA interactions, DNA methylation and gene expression
DNMT1-interacting RNAs block gene-specific DNA methylation.
Cell line, Subject
View SamplesThe epicardium, an epithelium covering the heart, is essential for cardiac development. During embryogenesis, the epicardium provides instructive signals for the growth and maturation of cardiomyocytes and for coronary angiogenesis. We generated an in vitro model of human embryonic epicardium derived from human pluripotent stem cells (hPSC-epi). These cells were able to differentiate into cardiac fibroblasts (cf) and smooth muscle cells (smc) in vitro (hPSC-epi-cf and hPSC-epi-smc respectively). Furthermore, we showed that they improved maturation of hPSC-derived cardiomyocytes (hPSC-cardio) in vitro while neural crest cells derived from hPSC (hPSC-NC) could not. Furthermore, they improved survival of hPSC-cardio and stimulated angiogenesis when injected in a rat model of myocardium infarction. We performed mRNA sequencing of the hPSC-epi, hPSC-epi-cf, hPSC-smc and hPSC-NC in order to identify the secreted molecules specifically produced by the hPSC-epi and/or its derivatives in comparison with the hPSC-NC. Vascular smooth muscle cells have different embryonic origins and different properties depending on their location in the body. The coronary smooth muscle cells come from the epicardium while the aortic ones come from the mesoderm or the neural crest. We performed mRNA sequencing of human coronary artery smc and human aortic smc to identify a specific signature of the coronary smc. We also compared the genes expressed in the hPSC-epi-smc and the smc derived from hPSC-derived lateral plate mesoderm. Overall design: For hPSC-derived samples the three replicates are coming from three different in vitro differentiations from H9. For the human primary cells, the triplicates are technical replicates (three different wells from the same culture at the same passage)
Epicardial cells derived from human embryonic stem cells augment cardiomyocyte-driven heart regeneration.
Specimen part, Subject
View SamplesSplenic innate-like marginal zone B (MZB) cells are strategically positioned at the interface between the circulating blood and lymphoid tissue, where they initiate rapid immune responses to blood-borne antigens. Here, we find that selective genetic deletion of MZB cells substantially increases the follicular helper T (Tfh) cell and germinal center (GC) response to high cholesterol diet (HCD), which leads to T cell-dependent acceleration of atherosclerosis. We show that MZB cells activate a homeostatic program in response to HCD, in which upregulation of the transcription factor Atf3 plays a determinant regulatory role. Shuttling of MZB cells to the follicle is dispensable for their regulatory properties on Tfh cells. Instead, HCD promotes increased interaction between MZB and (pre-)Tfh cells outside the follicle, and upregulates MZB cell expression of Cd274 in an Atf3-dependent manner. Interaction between MZB and Tfh cells leads to Cd274-mediated suppression of Tfh cell motility, limits Tfh cell accumulation in the follicle and suppresses the pro-atherogenic Tfh/GC response. Our findings reveal a previously unsuspected role for MZB cells in the control of Tfh/GC response to a cholesterol diet, and uncover a new mechanism through which MZB cells can couple their unique metabolic and innate immune properties and use them to maintain a tolerogenic state. The results may have broad (patho)physiological implications. Overall design: Transcriptomic comparision between high-fat diet and standard chow in LDLr -/- splenic marginal zone B cells
Marginal zone B cells control the response of follicular helper T cells to a high-cholesterol diet.
No sample metadata fields
View SamplesAneuploidy, i.e., variation in the number of individual chromosomes (chromosomal aneuploidy) or chromosome segment (segmental aneuploidy) is associated with developmental abnormalities and reduced fitness in all species examined, is the leading cause of miscarriages and mental retardations and a hallmark of cancer. Despite their documented importance in disease the effects of aneuploidies on the transcriptome remains largely unknown. Here we have examined the expression output in seven deficiency heterozygotes as single deficiencies and in all pairwise combinations. The results show that genes in one copy are buffered, i.e., are expressed above the expected 50% expression level compared to wild type and the buffering is general and not influenced by additional haploid regions. Long genes are significantly better buffered than short genes and our analysis suggests that gene length is the primary determinant for the degree of buffering. For short genes the degree of buffering depends on expression level and expression pattern. Furthermore, the results show that in deficiency heterozygotes the expression of genes involved in proteolysis is enhanced and negatively correlates with the degree of buffering. Our results suggest that proteolysis is a general response induced by aneuploidy.
Buffering and proteolysis are induced by segmental monosomy in Drosophila melanogaster.
Sex
View SamplesAll highly and poorly permeable metastases from the same mouse brain were collected by laser capture microdissection. Total RNA from both metastatic lesions and immediate microenvironment was isolated from 5 mice bearing 231-BR metastases. As control 4 healthy mouse brains were included.
Reactive astrocytic S1P3 signaling modulates the blood-tumor barrier in brain metastases.
Subject
View Samples