Obesity is associated with insulin resistance and increased intrahepatic triglyceride (IHTG) content, which are key risk factors for diabetes and cardiovascular disease. However, a subset of obese people does not develop these metabolic complications. We tested the hypothesis that MNO, but not MAO, people are protected from the adverse metabolic effects of weight gain. To this end, global transcriptional profile in adipose tissue before and after weight gain was evaluated by microarray analyses.
Metabolically normal obese people are protected from adverse effects following weight gain.
Specimen part
View SamplesThe purpose of this study was to evaluate the effect of progressive weight loss (5, 10, 15% weight loss) on metabolic function such as multi-organ insulin sensitivity and beta-cell function in obese people. We conducted microarray analysis to determine the effect of progressive weight loss on adipose tissue gene expression profile.
Effects of Moderate and Subsequent Progressive Weight Loss on Metabolic Function and Adipose Tissue Biology in Humans with Obesity.
Specimen part
View SamplesThe lack of accurate in vitro assays for predicting in vivo toxicity of chemicals together with new legislations demanding replacement and reduction of animal testing has triggered the development of alternative methods. This study aimed at developing a transcriptomics-based in vitro prediction assay for in vivo genotoxicity. The transcriptomics changes induced in the human liver cell line HepG2 by 34 compounds after treatment for 12h, 24h and 48h were used for the selection of gene-sets that can discriminate between in vivo genotoxins (GTX) and in vivo non-genotoxins (NGTX). By combining publicly available results for these chemicals from standard in vitro genotoxicity studies with transcriptomics, we developed several prediction models. These models were validated by means of an additional set of 28 chemicals.
A transcriptomics-based in vitro assay for predicting chemical genotoxicity in vivo.
Cell line, Time
View SamplesExpression of the proendocrine gene neurogenin 3 (Ngn3) is required for the development of pancreatic islets. In order to better characterize the molecular events regulated by Ngn3 during development, we have determined the expression profile of differentiating murine embryonic stem cells (mESCs) uniformly induced to overexpress Ngn3. An ESC line was created that allows for the induction of Ngn3 by adding doxycycline (Dox) to the culture medium. Genome-wide microarray analysis was performed to identify genes regulated by Ngn3 in a variety of both undifferentiated and differentiated conditions. Characterization of pancreatic developmental markers during embryoid body (EB) formation revealed an optimum context for Ngn3 induction. Neuroendocrine genes including neurogenic differentiation 1 (NeuroD1) and single minded 1 (Sim1) were found to be significantly upregulated. Genes regulated by Ngn3 independent of the context were analyzed using systematic gene ontology tools and revealed Notch signaling as the most significantly regulated signaling pathway (p=0.009). This result is consistent with the hypothesis that Ngn3 expression makes the cell competent for Notch signaling to be activated and conversely, more sensitive to Notch signaling inhibition. Indeed, EBs induced to express Ngn3 were significantly more sensitive to gamma-secretase inhibitor-mediated Notch signaling inhibition (p<0.0001). Moreover, we find that Ngn3 induction in differentiating ESCs results in significant increases in insulin, glucagon, and somatostatin transcription.
Differentiation of embryonic stem cells conditionally expressing neurogenin 3.
No sample metadata fields
View SamplesIn this experiment we compared total RNA from two commonly used choriocarcinoma cell lines, JEG3 and BeWo, to identify differentially expressed transcripts.
Microarray analysis of BeWo and JEG3 trophoblast cell lines: identification of differentially expressed transcripts.
No sample metadata fields
View SamplesRecent studies of cortical pathology in secondary progressive multiple sclerosis have shown that a more severe clinical course and the presence of extended subpial grey matter lesions with significant neuronal/glial loss and microglial activation are associated with meningeal inflammation, including the presence of lymphoid-like structures in the subarachnoid space in a proportion of cases. To investigate the molecular consequences of pro-inflammatory and cytotoxic molecules diffusing from the meninges into the underlying grey matter, we carried out gene expression profiling analysis of the motor cortex from 20 post-mortem multiple sclerosis brains with and without substantial meningeal inflammation and 10 non-neurological controls. Gene expression profiling of grey matter lesions and normal appearing grey matter not only confirmed the substantial pathological cell changes, which were greatest in multiple sclerosis cases with increased meningeal inflammation, but also demonstrated the upregulation of multiple genes/pathways associated with the inflammatory response. In particular, genes involved in tumour necrosis factor (TNF) signalling were significantly deregulated in MS cases compared to controls.
Meningeal inflammation changes the balance of TNF signalling in cortical grey matter in multiple sclerosis.
Specimen part, Disease, Disease stage
View SamplesWe identified distict mesodermal sub-populations based on Endoglin (Eng) and Flk1 expression in Brachyury (Bry) positive cells. By using whole-transcriptome analysis, we further characterized these populations and how they changed when Wnt pathway is inhibited Overall design: Reaggregates mRNA profiles of unsorted, Flk1+ Eng+, and Flk1- Eng+ samples were generated by deep sequencing, in triplicate , using Ilumina.
Endoglin integrates BMP and Wnt signalling to induce haematopoiesis through JDP2.
Specimen part, Treatment, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Restriction of intestinal stem cell expansion and the regenerative response by YAP.
Specimen part, Treatment
View SamplesRSpondin1 adenovirus was administered to mice and intestine was isolated for expression analysis 1 week later.
Restriction of intestinal stem cell expansion and the regenerative response by YAP.
Specimen part, Treatment
View SamplesSkeletal myogenic commitment of human pluripotent cells can be achieved by doxycycline-inducible expression of the transcription factor PAX7. To gain further insights on PAX7 function during this process, we performed a time course whole transcriptome analysis of differentiating H9 human embryonic stem cells from doxycycline-treated and untreated cultures. In addition, we identified the genomic binding of PAX7 in one of the selected time point (referred as PAX7+ proliferating myogenic progenitors). Overall design: Gene expression profiling was performed on biological replicates from differentiating H9 cells at the following time points: PAX7+ mesodermal cells (day 14), PAX7+ proliferating myogenic progenitors (approximately day 23), and differentiated myocytes (differentiation stage – around day 30; 7 days in the absence of PAX7 induction). Since PAX7 expression is doxycycline inducible, we also collected uninduced control samples at the same time points (termed mesodermal cells for day 14 and proliferating cells for day 23). PAX7 genomic binding was assessed in day 23 dox-treated cultures.
PAX7 Targets, CD54, Integrin α9β1, and SDC2, Allow Isolation of Human ESC/iPSC-Derived Myogenic Progenitors.
No sample metadata fields
View Samples