This SuperSeries is composed of the SubSeries listed below.
Amygdalar MicroRNA-15a Is Essential for Coping with Chronic Stress.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Integrated epigenome profiling of repressive histone modifications, DNA methylation and gene expression in normal and malignant urothelial cells.
Specimen part, Cell line
View SamplesTo gain a more depth knowledge of repressive epigenetic gene regulation in UCC, we have profiled H3K9m3 and H3K27m3 in normal and malignant urothelial cells. We matched these profiles to those 5-methylcytosine and gene expression. We hypothesized that differences represent pro-carcinogenic events within the urothelium.
Integrated epigenome profiling of repressive histone modifications, DNA methylation and gene expression in normal and malignant urothelial cells.
Specimen part, Cell line
View SamplesUrothelial cell carcinoma of the bladder (UCC) is a common disease characterized by FGFR3 mutation. Whilst upregulation of this oncogene occurs most frequently in low-grade non-invasive tumors, recent data reveal increased FGFR3 expression characterizes a common sub-type of invasive UCC sharing genetic similarities with lobular breast cancer. These similarities include upregulation of the FOXA1 transcription factor and reduced expression of microRNAs-99a/100. We have previously identified direct regulation of FGFR3 by these two microRNAs and now search for further targets. Using a microarray meta-database we find potential FOXA1 regulation by microRNAs-99a/100. We confirm direct targeting of the FOXA1 3UTR by microRNAs-99a/100 and also potential indirect regulation through microRNA-485-5p/SOX5/JUN-D/FOXL1 and microRNA-486/FOXO1a. In 292 benign and malignant urothelial samples, we find an inverse correlation between the expression of FOXA1 and microRNAs-99a/100 (r=-0.33 to -0.43, p<0.05). As for FGFR3 in UCC, tumors with high FOXA1 expression have lower rates of progression than those with low expression (Log rank p=0.009). Using global gene expression and CpG methylation profiling we find genotypic consequences of FOXA1 upregulation in UCC. These are associated with regional hypomethylation and near FOXA1 binding sites, and mirror patterns previously reported in FGFR3 mutant UCC. These include gene silencing through aberrant hypermethylation (e.g. IGFBP3) and affect genes that characterize lobular breast cancer (e.g. ERBB2, XBP1). In conclusion, we have identified microRNAs-99a/100 mediate a direct relationship between FGFR3 and FOXA1, and potentially facilitate cross talk between these pathways in UCC.
MicroRNA-99a and 100 mediated upregulation of FOXA1 in bladder cancer.
Cell line
View SamplesThere is much evidence that T cells may be activated via mechanisms which act independently of direct TCR ligation. Despite this, the question of whether such forms of bystander T cell activation occur during immune responses is hotly debated.
Human CD4+ memory T cells are preferential targets for bystander activation and apoptosis.
No sample metadata fields
View SamplesOne of the hallmarks in hypertension is a pressure-induced change in endothelial cell phenotype. A cytoskeletal protein zyxin, which was seen to translocate from focal adhesion contacts to the nucleus in response to the increased wall tensionis, mediates the tension-induced endothelial signaling.
Zyxin mediation of stretch-induced gene expression in human endothelial cells.
Specimen part
View SamplesRNAseq analysis of cell lines with ADAR1-p150 and ADAR1-p110 knock-outs and primary human tissue samples (from GSE57353 and GSE99392 data sets) to identify sites of ADAR1 editing Overall design: 12 samples: 3 cell lines (HeLa, HeLa-p150KO, HeLa-ADAR1KO) with four conditions each (no treatment, MeV-vac2(GFP)-infected, MeV-CKO(GFP)-infected, IFNA/D-treated). One biological replicate per sample. In addition, raw data files of 9 samples from series GSE57353 and GSE99392 were re-analyzed using the same data processing pipeline.
Extensive editing of cellular and viral double-stranded RNA structures accounts for innate immunity suppression and the proviral activity of ADAR1p150.
Cell line, Subject
View SamplesStearoyl-CoA desaturase (SCD) is the rate-limiting enzyme catalyzing the conversion of saturated fatty acids palmitate and stearate to monounsaturated fatty acids palmitoleate and oleate. During adipocyte differentiation, SCD expression increases concomitantly with several transcription factors and lipogenic genes.
Inhibition of stearoyl-CoA desaturase-1 in differentiating 3T3-L1 preadipocytes upregulates elongase 6 and downregulates genes affecting triacylglycerol synthesis.
Specimen part, Treatment
View SamplesThe goal of this study was to determine if blood circulating monocytes of metastatic breast cancer patient would express a different activation profile compared to healthy donors, in order to use this specific changesas biomarkers to monitor then response to therapy Overall design: CD11b+ cells were extracted from all blood of 4 healthy donors and 4 metastatic breast cancer patients using magnetic beads separation (Miltenyi). CD11b+ cells were then lysed and mRNA was extracted to perform RNASeq.
Bevacizumab specifically decreases elevated levels of circulating KIT+CD11b+ cells and IL-10 in metastatic breast cancer patients.
No sample metadata fields
View SamplesThe classical concept of bone marrow-derived mesenchymal stem cells (BM-MSC), intended as a uniform, broad potent population, is progressively being substituted by the idea that the bone marrow harbors heterogeneous populations of non-hematopoietic stem cells. This in vivo heterogeneity is also amplified by the different experimental strategies used to isolate/culture them. Among the exogenous factors described to affect MSC in vitro growth, basic-fibroblast growth factor (bFGF) is one of the most common growth factors used to expand stem cells. Moreover, it has been reported that its signaling is associated with the mainteinance of stemness of a variety of stem cells, included MSC. Using an ectopic model of bone regeneration, we have previously described that the implantation of cells with different commitment levels, differentially influences the capacity to recruit host cells, activating endogenous regenerative mechanisms. Due to its properties, we here demonstrate that the addition of bFGF to primary BM cultures, leads to the selection of specific subpopulations able to induce a different host regenerative response, when in vivo implanted in association with suitable ceramic scaffolds. Moreover, taking advantage of a multiparametric and comparative genomic and proteomic approach, it has been evaluated how different culture conditions combine to bring about appreciable changes in the secretome of the cells, that consequently influence their in vivo regenerative behaviour. The full comprehension of the regulatory mechanisms that rule the host response depending on the type and differentiative stage of the transplanted cells could help us to develop novel clinical strategies where host cells could directly contribute to regenerate the appropriate tissue.
The role of bFGF on the ability of MSC to activate endogenous regenerative mechanisms in an ectopic bone formation model.
Specimen part, Disease
View Samples