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GSE29411
Homo sapiens
5 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Using gene expression to predict differences in the secretome of human omental vs. subcutaneous adipose tissue.
Sample Metadata Fields
Sex, Specimen part
View Samples- Homo sapiens
- 5 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The objective was to characterize differences in the secretome of human omental compared with subcutaneous adipose tissue using global gene expression profiling. Gene expression was measured using Affymetrix microarrays in subcutaneous and omental adipose tissue (n=3 independent subjects; 6 arrays). Predictive bioinformatic algorithms were employed to identify those differentially expressed genes that code for secreted proteins and to identify common pathways between these proteins. All patients provided informed written consent before inclusion in the study which was approved by the North of Scotland Research Ethics Committee (NOSREC).
Publication Title
Using gene expression to predict differences in the secretome of human omental vs. subcutaneous adipose tissue.
Sample Metadata Fields
Sex, Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
Illumina HiSeq 1000
Description
Background: Global DNA methylation contributes to genomic integrity by supressing repeat associated transposition events. Several chromatin factors are required in addition to DNA methyltransferases to maintain DNA methylation at intergenic and satellite repeats. Embryos lacking Lsh, a member of the SNF2 superfamily of chromatin helicases, are hypomethylated. The interaction of Lsh with the de novo methyltransferase, Dnmt3b, facilitates the deposition of DNA methylation at stem cell genes. We wished to determine if a similar targeting mechanism operates to maintain DNA methylation at repetitive sequences. Results: We used HELP-seq to map genome wide DNA methylation patterns in Lsh-/- and Dnmt3b-/- somatic cells. DNA methylation is predominantly lost from specific genomic repeats in Lsh-/- cells: LTR-retrotransposons, LINE-1 repeats and mouse satellites. RNA-seq experiments demonstrate that specific IAP (Intracisternal A-type particle) LTRs and satellites, but not LINE-1 elements, are aberrantly transcribed inLsh-/- cells. LTR hypomethylation in Dnmt3b-/- cells is moderate and hypomethylated repetitive elements (IAP, LINE-1 and satellite) are silent. Chromatin immunoprecipitation (ChIP) indicates that repressed LINE-1 elements gain H3K4me3, but H3K9me3 levels are unaltered in Lsh-/- cells, indicating that DNA hypomethylation alone is not permissive for their transcriptional activation. Mis-expressed IAPs and satellites lose H3K9me3 and gain H3K4me3 in Lsh-/- cells. Conclusions: Our study emphasizes that regulation of repetitive elements by DNA methylation is selective and context dependent. We propose a model where Lsh is specifically required at a precise developmental window to target de novo methylation to repeat sequences, which is subsequently maintained by Dnmt1 in somatic cells to enforce repeat silencing thus contributing to genomic integrity. Overall design: Two pairs of RNA samples compared: WT and Lsh-/- RNA isolations from tail-tip fibroblasts; WT and Lsh-/- RNA isolations from E13.5 mouse embryos.
Publication Title
Lsh regulates LTR retrotransposon repression independently of Dnmt3b function.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cellular senescence is a stable proliferation arrest in response to stress, associated with an altered secretory pathway (Senescence Associated Secretory Phenotype (SASP)). Senescence-associated proliferation arrest and the SASP are thought to act in concert to promote tumor suppression and tissue aging. While chromatin regulation and down regulation of lamin B1 have been implicated as effectors of cell senescence, functional interactions between them are poorly understood. We compared the genome-wide distributions of H3K4me3 and H3K27me3 between proliferating and senescent primary human cells and found dramatic differences, including large-scale domains of H3K4me3- and H3K27me3-enriched mesas and H3K27me3-depleted canyons in senescent cells. Senescent mesas form at the sites of lamin B1-associated domains (LADs) in proliferating cells. Mesas also overlap with regions that exhibit DNA hypomethylation in cancer, suggesting that chromatin changes in pre-malignant senescent cells foreshadow epigenetic changes in cancer. Proliferating fibroblasts from Hutchinson-Gilford Progeria Syndrome patients expressing mutant lamin A (progerin) also show evidence of H3K4me3 mesas, suggesting a link between premature chromatin changes and accelerated cell senescence and tissue aging. In contrast, canyons form mostly in between LADs and are enriched in genes, gene promoters and enhancers. Strikingly, H3K27me3 loss in canyons is correlated with upregulation of key senescence genes, including genes comprising the SASP, indicating a link between global changes in chromatin structure and local regulation of gene expression. Finally, premature reduction of lamin B1 in midlife proliferating cells triggers formation of senescence-associated mesas and canyons and accelerated senescence. Together, our data illustrate a profound reorganization of chromatin during senescence, and suggest that down regulation of lamin B1 in senescence is a key trigger of global and local chromatin changes that impact gene expression, aging and cancer.
Publication Title
Lamin B1 depletion in senescent cells triggers large-scale changes in gene expression and the chromatin landscape.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 248 Downloadable Samples
- Illumina HiSeq 2000
Description
Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality, is primarily caused by prolonged exposures to cigarette smoke (CS) and the disease may persist or progress even after smoking cessation. To provide novel insight the mechanisms of COPD development we investigated temporal patterns of lung transcriptome expression in response to chronic CS exposure that also persist following CS cessation, using next generation sequencing techniques. Whole lung RNA-seq data was analyzed from C57Bl/6 mice exposed to CS for 1 day, 7 days, 1 month, 3 months, 6 months, and 9 months as well as for 6 months followed by 3 months of cessation. Age-matched littermate mice exposed to ambient air were used as control (AC). Differential gene expression and pathway analyses revealed consistent upregulation of genes involved in glutathione metabolism, a pathway previously implicated in lung responses to chronic CS and in COPD, that was reversible upon cessation. In addition, novel patterns in mouse-model pathways such as pyrimidine metabolism and phosphatidylinositol signaling system and have been recognized. Genes in these pathways encoding for enzymes controlling metabolic functions were significantly altered by CS exposures and were associated with congruent abnormalities in contemporaneous plasma metabolomic profiles. The bioinformatics integration of lung tissue genomics and plasma metabolomics uncovered that changes in lung gene expression induced by CS exposures are translated in systemic metabolic signatures, with potential implication in the development of COPD. Overall design: Whole transcriptome profiling of air control vs cigarette smoke-exposed mice at each of 6 timepoints from 1 day to 9 months of exposure, including a stop smoking group exposed to 6 months of CS followed by 3 months of ambient air recovery. Each treatment-by-time experimental group contains 5 biological replicates. 3 samples were discarded for quality reasons.
Publication Title
Gene and metabolite time-course response to cigarette smoking in mouse lung and plasma.
Sample Metadata Fields
Specimen part, Cell line, Treatment, Subject, Time
View Samples- Homo sapiens
- 10 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Standardization of MSC manufacturing is urgently needed to facilitate comparison of clinical trial results. Here, we compare gene expression of MSC generated by the adaptation of a proprietary method for isolation and cultivation of a specific umbilical cord tissue-derived population of Mesenchymal Stromal Cells (MSCs)
Publication Title
Towards an advanced therapy medicinal product based on mesenchymal stromal cells isolated from the umbilical cord tissue: quality and safety data.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 106 Downloadable Samples
- Affymetrix Human Genome U219 Array (hgu219)
Description
We analyzed total leukocyte gene expression using Affymetrix microarrays from healthy smokers, COPD patients and non-smoking control subjects before and after exposure to acute cigarette smoke (smoking two cigarettes in 30 minutes).
Publication Title
Systemic inflammatory response to smoking in chronic obstructive pulmonary disease: evidence of a gender effect.
Sample Metadata Fields
Sex, Specimen part, Disease
View Samples- Homo sapiens
- 12 Downloadable Samples
- Affymetrix Human Transcriptome Array 2.0 (hta20)
Description
In order to explore the funciton of p53 splice variant in DNA damage response, we utilized CRISPR-cas9 genome editing technique to specifically knock out this variant in MCF7 cells.
Publication Title
Identification of a DNA Damage-Induced Alternative Splicing Pathway That Regulates p53 and Cellular Senescence Markers.
Sample Metadata Fields
Treatment
View Samples- Saccharomyces cerevisiae
- 15 Downloadable Samples
- Affymetrix Yeast Genome 2.0 Array (yeast2)
Description
Gene expression in eukaryotes is an essential process that includes transcription, pre-RNA processing and RNA export. All these steps are coupled and normally, any failure in one step affects the other steps and could cause nuclear mRNA retention. One important player in this interface is the poly(A)-RNA binding protein Nab2, which regulates the poly(A)-tail length of mRNAs protecting their 3-ends from a second round of polyadenylation and facilitating their nucleo-cytoplasmic export. Interestingly, here we show that Nab2 has additional roles in mRNA transcription elongation, tRNA metabolism and rRNA export.
Publication Title
Nab2 functions in the metabolism of RNA driven by polymerases II and III.
Sample Metadata Fields
No sample metadata fields
View Samples