Adipocyte precursor cells were treated with Pdgfa during 1 or 2 hours in vitro to identify early changes in transciprion in response to treatment. This experiment supports the evidence that Pdgfa induces proliferation and maintenance of adipocyte stem cells. Overall design: Adipocyte precursor cells were isolated by FACS and treated with 30ng/ml of recombinant mouse Pdgfa for 1 or 2 hours.
Skin Adipocyte Stem Cell Self-Renewal Is Regulated by a PDGFA/AKT-Signaling Axis.
Sex, Age, Specimen part, Cell line, Subject
View SamplesWe performed whole transcriptome profiling on sorted tissue macrophages from the spleen or from visceral adipose tissue (VAT) of wild-type mice that are 3-month or 24-month of age or from 24-month Nlrp3-/- mice Overall design: Profiles were generated on fluorescence-activated-cells (FACs) sorted F480+CD11b+ cells from spleen or adipose tissue, using sequencing analysis
Inflammasome-driven catecholamine catabolism in macrophages blunts lipolysis during ageing.
Sex, Age, Specimen part, Subject
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genome-wide analysis in human colorectal cancer cells reveals ischemia-mediated expression of motility genes via DNA hypomethylation.
Cell line, Treatment
View SamplesA great number of studies have investigated changes induced by morphine exposure in gene expression using several experimental models. In this study, we examined gene expression changes during chronic exposure to morphine during maturation and differentiation of zebrafish CNS.
Whole-genome expression profile in zebrafish embryos after chronic exposure to morphine: identification of new genes associated with neuronal function and mu opioid receptor expression.
Treatment
View SamplesDNA hypomethylation is an important epigenetic modification found to occur in many different cancer types, leading to the upregulation of previously silenced genes and loss of genomic stability. We previously demonstrated that hypoxia and hypoglycaemia (ischemia), two common micro-environmental changes in solid tumors, decrease DNA methylation through the downregulation of DNMTs in human colorectal cancer cells. Here, we utilized a genome-wide cross-platform approach to identify genes hypomethylated and upregulated by ischemia. Following exposure to hypoxia or hypoglycaemia, methylated DNA from human colorectal cancer cells (HCT116) was immunoprecipitated and analysed with an Affymetrix promoter array. Additionally, RNA was isolated and analysed in parallel with an Affymetrix expression array. Ingenuity pathway analysis software revealed that a significant proportion of the genes hypomethylated and upregulated were involved in cellular movement, including PLAUR and CYR61. A Matrigel invasion assay revealed that indeed HCT116 cells grown in hypoxic or hypoglycaemic conditions have increased mobility capabilities. Confirmation of upregulated expression of cellular movement genes was performed with qPCR. The correlation between ischemia and metastasis is well established in cancer progression, but the molecular mechanisms responsible for this common observation have not been clearly identified. Our novel results suggest that hypoxia and hypoglycaemia may be driving changes in DNA methylation through downregulation of DNMTs. This is the first report to our knowledge that provides an explanation for the increased metastatic potential seen in ischemic cells; i.e. that ischemia could be driving DNA hypomethylation and increasing expression of cellular movement genes.
Genome-wide analysis in human colorectal cancer cells reveals ischemia-mediated expression of motility genes via DNA hypomethylation.
Cell line, Treatment
View SamplesChronic tendon injuries, also known as tendinopathy, are common among professional and recreational athletes. These injuries result in a significant amount of morbidity and health care expenditure and yet little is known about the molecular mechanism leading to tendinopathy. We have used histological evaluation and molecular profiling to determine the gene expression changes in 23 human patients undergoing surgical procedures for the treatment of chronic tendinopathy. Diseased tendons have altered extracellular matrix, fiber disorientation, increased cellular content and vasculature and the absence of inflammatory cells. Global gene expression profiling identified 1783 transcripts with significant different expression patterns in the diseased tendons. Global pathway analysis further suggests altered expression of extracellular matrix proteins and the lack of an appreciable inflammatory response. We have identified pathways and genes regulated in tendinopathy samples that will help contribute to the understanding of the disease towards the development of novel therapeutics.
Regulation of gene expression in human tendinopathy.
Sex, Age, Specimen part, Disease, Disease stage, Subject
View SamplesImmunoprecipitation of EGFR from irradiated A549 (ATCC CCL185) cells was performed in order to characterize bound mRNA species with the help of microarray analysis
New roles for nuclear EGFR in regulating the stability and translation of mRNAs associated with VEGF signaling.
Cell line, Treatment
View SamplesRecent advances in multiple whole genome technologies provide unprecedented opportunities to profile epigenomic signatures in cancer cells. Previously we used a human gene promoter tiling microarray platform to identify genome-wide DNA methylation changes in a cell line model of breast cancer metastasis. Interestingly, the clustered nature of epigenetic targets that we identified, along with our concurrent karyotype analyses, have now led us to hypothesize that complex genomic alterations in cancer cells (deletions, translocations and ploidy) may be superimposed over promoter-specific methylation events that are responsible for gene-specific expression changes.
Multi-platform whole-genome microarray analyses refine the epigenetic signature of breast cancer metastasis with gene expression and copy number.
Cell line
View Samplesp53 induces cell death upon DNA damage, but this may not confer all of its tumor suppressor activity. We report that p53 activation enhances the processivity of DNA replication, as monitored by multi-label fiber assays, whereas removal of p53 reduces fork progression. This was observed in tumor-derived U2OS cells, but also in murine embryonic fibroblasts with heterozygous or homozygous p53 deletion, and in freshly isolated thymocytes from mice with differential p53 status. Mdm2, a p53-inducible gene product, similarly supported DNA replication even in p53-deficient cells, suggesting that sustained Mdm2-expression is at least one of the mechanisms allowing p53 to prevent replicative stress. Thus, p53 helps to protect the genome during S phase, by preventing the occurrence of stalled or collapsed replication forks. These results expand p53’s tumor-suppressive functions, adding to the ex-post model (elimination of damaged cells) an ex-ante activity, i.e. the prevention of DNA damage during replication. Overall design: Expression profiling by high throughput sequencing
p53 Activity Results in DNA Replication Fork Processivity.
Specimen part, Cell line, Subject
View SamplesMicroarray analysis revealed that changes in genes expressions are brain region-dependent; expression of several genes are affected by point mutation L100P, which was verified by RT-PCR (Lcn2, Cyr61, Slc6a12, Slc40a1, Egr2), a few genes are affected by genotype and valproate (Dusp1 and Purb), suggesting their role in valproate-induced benificial effect on sensorimotor gaiting in Disc1-L100P mutant mice. The final conclusion will be drawn after series of RT-PCR confirmation.
Genetic and pharmacological evidence for schizophrenia-related Disc1 interaction with GSK-3.
Sex, Specimen part, Compound
View Samples