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GSE59930
Mus musculus
9 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Major causes of lipid accumulation in liver are increased import, synthesis or decreased catabolism of fatty acids. The latter is caused by dysfunction of cellular organelle controlling energy homeostasis, i.e. mitochondria. However, peroxisomes appear to be an important organelle in lipid metabolism of hepatocytes, but little is known about their role in the development of non-alcoholic fatty liver disease (NAFLD). To investigate the role of peroxisomes next to mitochondria in excessive hepatic lipid accumulation we used the leptin resistant db/db mice on C57BLKS background, a mouse model that develops hyperphagia induced diabetes with obesity and NAFLD.
Publication Title
Peroxisomes compensate hepatic lipid overflow in mice with fatty liver.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Homo sapiens
- 6 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The SKOV-3 and Caov-3 ovarian cancer cell lines where seeded onto the 100mm cell culture plate for overnight. The cells were then incubated with IL-6 (30ng/ml) alone for one hour or pre-treated with siltuximab for four hours and then treated with IL-6 for one hour. Total RNA was collected from these cells using TRIzol Reagent (GIBCO Grand Island, NY) according to the manufacturers instructions. To account for and eliminate biologic noise, RNA was isolated from three distinct flasks of each cell line and pooled together. RNA quality was determined via ethidium bromide staining following agarose/formaldehyde gel electrophoresis. Total RNA was processed and hybridized to Affymetrix Genechip HG-U95Av2 arrays (Affymetrix, Santa Clara, CA) by the Gene Array Technology Center at Harvard Medical School (http://genome.med.harvard.edu). Affymetrix Gene Chip U133 Plus 2.0 in the first and most comprehensive whole human genome expression array. This array completes coverage of the whole human Genome with over 47,000 transcripts. The expression level of each mRNA is quantified by measuring its hybridization to these 23-mers in comparison to its hybridization to a one-base mismatch oligonucleotide. GeneSifter was used to analyze the microarray data (http://www.genesifter.net/web/). Fold change in expression between sensitive and resistant cell lines was evaluated using the Mann-Whitney test. A tenfold or greater change in intensity combined with a Mann-Whitney associated P value less than 0.05 was used as the criterion for inclusion in our filtered data set.
Publication Title
Effects of siltuximab on the IL-6-induced signaling pathway in ovarian cancer.
Sample Metadata Fields
Specimen part, Cell line
View Samples- Mus musculus
- 2 Downloadable Samples
Illumina HiSeq 2000
Description
about 250 genes were significantly changed after Gata4 and Gata6 were specifically deleted in the pancreatic progenitor cells Overall design: 6 pancreatic buds were pooled for the control, and 12 pancreatic buds were pooled for the Pdxcre; Gata4fl/fl; Gata6fl/fl. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq
Publication Title
GATA4 and GATA6 regulate pancreatic endoderm identity through inhibition of hedgehog signaling.
Sample Metadata Fields
Specimen part, Disease, Subject
View Samples- Homo sapiens
- 43 Downloadable Samples
- Illumina HiSeq 2000
Description
Hepatitis C virus (HCV) is widely used to investigate host-virus interactions and cellular responses to infection have been extensively studied in vitro. In human liver, interferon (IFN) stimulated gene expression can mask direct transcriptional responses to virus infection. To better characterize the direct effects of HCV infection in vivo, we analyze the transcriptomes of HCV-infected patients lacking an activated endogenous IFN system. We show that the expression changes observed in these patients predominantly reflect immune cell infiltrates rather than changes in cell-intrinsic metabolic pathways. We also investigate the transcriptomes of patients with endogenous IFN activation, which paradoxically cannot eradicate viral infection. We find that most IFN-stimulated genes (ISGs) are induced by both the endogenous IFN system and by recombinant IFN therapy, but with significantly higher induction levels in the latter. We conclude that the innate host immune response in chronic hepatitis C is too weak to clear the virus. Overall design: In this study, we aimed to disentangle the direct and indirect effects of HCV infection on cellular transcriptional profiles, by performing a detailed characterization of the gene expression changes associated with HCV infection, endogenous IFN system activation and pegIFNa treatment in the human liver. With this objective, we generated and analyzed high-throughput transcriptome sequencing profiles from liver biopsies derived from different categories of HCV-infected and non-infected patients, prior to and during treatment. First, to unveil HCV-induced cell-autonomous effects and to separate them from IFN-induced changes in the transcriptome, we selected liver biopsies from patients with chronic hepatitis C (CHC) without hepatic ISG induction, and compared them with un-infected control biopsies. Second, we examined the transcriptomic changes associated with the endogenous activation of the IFN system. Finally, we analyzed the gene expression changes resulting from pegIFNa/ribavirin treatment, by comparing transcriptome data from liver biopsies obtained before treatment and at different time points during the first week of therapy.
Publication Title
Transcriptional response to hepatitis C virus infection and interferon-alpha treatment in the human liver.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Drosophila melanogaster
- 6 Downloadable Samples
- Affymetrix Drosophila Genome 2.0 Array (drosophila2)
Description
Examined the expression effects of supplementing Drosophila food on heart and nephrocyte complexes
Publication Title
Diet-Induced Podocyte Dysfunction in Drosophila and Mammals.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples- Mus musculus
- 9 Downloadable Samples
- Illumina HiSeq 2000
Description
We report the transcriptome changes that result of the genomic deletion of one or two alleles of an islet-specific long non-coding RNA (Blinc1) in isolated pancreas from e15.5 mouse embryos. Overall design: Pancreas from e15.5 embryos were dissected and total RNA extracted. Libraries were prepared from total RNA (RIN>8) with the TruSeq RNA prep kit (Illumina) and sequenced using the HiSeq2000 (Illumina) instrument. More than 20 million reads were mapped to the mouse genome (UCSC/mm9) using Tophat (version 2.0.4) with 4 mismatches and 10 maximum multiple hits. Significantly differentially expressed genes were calculated using DEseq.
Publication Title
βlinc1 encodes a long noncoding RNA that regulates islet β-cell formation and function.
Sample Metadata Fields
Specimen part, Subject
View Samples- Homo sapiens
- 66 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Transcriptome analysis of human diabetic kidney disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 24 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Publication Title
Transcriptome analysis of human diabetic kidney disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 20 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Publication Title
Transcriptome analysis of human diabetic kidney disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage, Subject
View Samples- Homo sapiens
- 22 Downloadable Samples
- Affymetrix Human Genome U133A 2.0 Array (hgu133a2)
Description
We identified 1,700 differentially expressed probesets in DKD glomeruli and 1,831 in diabetic tubuli; 330 probesets were commonly differentially expressed in both compartments. The canonical complement signaling pathway was determined to be statistically differentially regulated in both DKD glomeruli and tubuli and was associated with increased glomerulosclerosis even in an additional set of DKD samples.
Publication Title
Transcriptome analysis of human diabetic kidney disease.
Sample Metadata Fields
Specimen part, Disease, Disease stage
View Samples