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GSE24132
Homo sapiens
12 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Respiratory syncytial virus (RSV) is a major cause of morbidity and mortality. Previous studies have suggested that T cell responses may contribute to RSV immunopathology, which could be driven by dendritic cells (DCs). DCs are productively infected by RSV, and during RSV infections, there is an increase of DCs in the lungs with a decrease in the blood. Pediatric populations are particularly susceptible to severe RSV infections, however DC responses to RSV from pediatric populations have not been examined. In this study, primary isolated DCs from cord blood and adult peripheral blood were compared after RSV-infection. Transcriptional profiling and biological network analysis identified transforming growth factor (TGF)-b and associated signaling molecules as differentially regulated in the two age groups. TGF-b1 was decreased in RSV-infected adult blood DCs, but increased in RSV-infected cord blood DCs. Co-culture of adult RSV-infected DCs with autologous T-cells induced secretion of interferon gamma (IFNg), IL-12p70, IL-2, and tumor necrosis factor alpha (TNFa). Conversely, co-culture of cord RSV-infected DCs and autologous T-cells induced secretion of IL-4, IL-6, IL-1b, and IL-17. Addition of purified TGF-b1 to adult DC-T cell co-cultures reduced secretion of IFNg, IL-12p70, IL-2, and TNFa, which addition of a TGF-b chemical inhibitor to cord DC-T cell co-cultures increased secretion of IL-12p70. These data suggest that TGF-b acts as a major regulator of RSV DC-T cell responses, which could contribute to immunopathology during infancy.
Publication Title
Transforming growth factor beta is a major regulator of human neonatal immune responses following respiratory syncytial virus infection.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
WNT5A inhibits metastasis and alters splicing of Cd44 in breast cancer cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
A highly metastatic breast cancer cell line, 4T1, was used to generate stable Wnt5a expressing and vector only control cells. Cells were generated using lentivirus infection and selection with blasticidin. Expression of Wnt5a was confirmed using western blot. Cell behaviour was characterized. Wnt5a expressing cells exhibited reduced migration in a transwell assay and reduced metastasis in a tail vein injection assay. Growth was not significantly affected.
Publication Title
WNT5A inhibits metastasis and alters splicing of Cd44 in breast cancer cells.
Sample Metadata Fields
Cell line
View Samples- Mus musculus
- 4 Downloadable Samples
NextSeq 500
Description
To investigate differential gene expression that might account for the differing glomerular phenotype of NPHS2-Cre +/+ mice when compared with wild-type control, including altered GBM thickness, loss of normal foot process morphology, and decrease in podocyte number, RNA sequencing analysis was performed on glomeruli extracted from both NPHS2-Cre +/+ and wild-type control mice. Overall design: Following isolation of glomeruli using Dynabeads from NPHS2-Cre +/+ and wild-type control mice (n=2 biological replicates per genotype, singly isolated), total RNA was extracted and RNA samples were submited for sample preparation and sequencing.
Publication Title
Podocyte-specific expression of Cre recombinase promotes glomerular basement membrane thickening.
Sample Metadata Fields
Sex, Age, Specimen part, Cell line, Subject
View Samples- Bos taurus
- 65 Downloadable Samples
- Illumina Genome Analyzer II
Description
Cellular mechanisms that contribute to low estradiol concentrations produced by the preovulatory ovarian follicle in cattle with a compromised metabolic status (such as lactatino) are largely unknown. To gain insight into the main metabolic mechanisms affecting preovulatory follicle function RNAseq profiling was conducted on non-lactating Holstein-Friesian heifers (n=16) and lactating Holstein-Friesian cows (n=17) at three stages of preovulatory follicle development: A) newly selected dominant follicle in the luteal phase (Selection); B) follicular phase before the LH surge (Differentiation) and C) pre-ovulatory phase after the LH surge (Luteinization). Based on a combination of RNA sequencing, ingenuity pathway analysis and Q-RT-PCR validation several important molecular markers involved in steroid biosynthesis, such as the expression of steroidogenic acute regulatory protein (STAR) within developing dominant follicles, were identified to be affected (downregulated) by the catabolic state. We propose that the adverse metabolic environment caused by lactation decreases preovulatory follicle function by affecting cholesterol transport into the mitochondria to initiate steroidogenesis. Overall design: Granulosa and Theca samples from the dominant follicle were taken from cows and heifers at stages: selection, differentiation and luteinization.
Publication Title
Effect of the metabolic environment at key stages of follicle development in cattle: focus on steroid biosynthesis.
Sample Metadata Fields
Specimen part, Subject
View Samples- Mus musculus
- 6 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Pofut1 is an essential gene that glycosylates proteins containing EGF-like repeats, including Notch Receptors (NotchRs). Work in mice and in Drosophila has shown that O-fucosylation by Pofut1 is required for NotchR ligands to bind to and activate NotchRs. As such, Pofut1 deletion in skeletal myofibers allows for an analysis of potential functions and molecular changes of Pofut1 in skeletal muscle that derive from its expression in skeletal myofibers. In this study we compared gene expression profiles between quadriceps muscles in mice where Protein O-fucosyltransferase 1 (Pofut1) was deleted specifically in skeletal myofibers via use of a human skeletal alpha actin Cre transgene (Scre) and a loxP flanked Pofut1 gene (SCreFF) and mice which bore the only the Scre transgene but did not have floxed Pofut1 alleles (SCre++).
Publication Title
Deletion of <i>Pofut1</i> in Mouse Skeletal Myofibers Induces Muscle Aging-Related Phenotypes in <i>cis</i> and in <i>trans</i>.
Sample Metadata Fields
Age, Specimen part
View Samples- Homo sapiens
- 14 Downloadable Samples
- IlluminaHiSeq2500
Description
It is well known that both recipient cells and donor nuclei demonstrate a mitotic advantage as observed in the traditional reprogramming with somatic cell nuclear transfer (SCNT). However, It is not known whether a specific mitotic factor plays a critical role in reprogramming. Here we identify an isoform of human bromodomain-containing 3 (BRD3), BRD3R (BRD3 with Reprogramming activity), as a reprogramming factor. BRD3R positively regulates mitosis during reprogramming, upregulates a large set of mitotic genes at early stages of reprogramming, and associates with mitotic chromatin. Interestingly, a set of the mitotic genes upregulated by BRD3R constitutes a pluripotent molecular signature. The two BRD3 isoforms display differential binding to acetylated histones. Our results suggest a molecular interpretation for the mitotic advantage in reprogramming, and show that mitosis may be a driving force of reprogramming. Overall design: Human BJ cells transduced with lentiviral particles of the conventional reprogramming factors (OCT3/4, SOX2 and KLF4) were used as controls. Two types of controls were used: 1) BJ transduced with OSK (OCT4, SOX2 and KFL4) viruses; 2) BJ cells transduced with OSK plus GFP viruses. Experimental treatment was BJ cells transduced with OSK plus BRD3R viruses. RNA was extracted from cells at day 3 of reprogramming because the reprogramming cells are still homogeneous and transgenes are well expressed at this time point.
Publication Title
The acetyllysine reader BRD3R promotes human nuclear reprogramming and regulates mitosis.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 4 Downloadable Samples
- IlluminaHiSeq2000
Description
Purpose: Cellular senescence is a cell stress response resulting in permanent growth arrest and the production of an altered pro-inflammatory secretory profile known as the senescecnce-associated secretory phenotype (SASP). The induction of senescence in astrocytes, a cell type responsible for maintaining homeostasis within the central nervous system (CNS) and responding to CNS insults, has been implicated in neurodegenerative disease. However, little is known about the senescent transcriptome in CNS-derived cell types including astrocytes. Methods: To better understand senescence-associated gene expression changes in astrocytes, we investigated global changes in the astrocyte transcriptome using RNA-seq following the induction of oxidative stress-induced senescence with hydrogen peroxide. Results: During senescence, we find evidence of a loss of brain expressed transcripts involved in diverse CNS processes including neuronal differentiation and development, gliogenesis, axonogenesis, and learning and memory as well as a loss of transcripts involved in MHC class II antigen processing and presentation. In addition, we find evidence for induction of the senescent phenotype including a loss of transcripts involved in cell division and an increase in the mRNA level of inflammatory mediators suggestive of a SASP. Conclusions: Overall, our findings suggest a loss of differentiated function in senescent astrocytes and a gain in neuroinflammatory function as part of the SASP as a potential mechanisms for dysfunction in the aging brain. Overall design: Examination of transcriptome changes by RNAseq in pre-senescent and senescent astrocytes using 2 biological replicates per condition
Publication Title
Changes in the Transcriptome of Human Astrocytes Accompanying Oxidative Stress-Induced Senescence.
Sample Metadata Fields
No sample metadata fields
View Samples- Mus musculus
- 8 Downloadable Samples
- Affymetrix Murine Genome U74A Version 2 Array (mgu74av2)
Description
Disruption of the mouse gene encoding the gap junction subunit alpha3 connexin 46 (Cx46) results in the formation of lens cataracts. The timing of the onset of this lens opacity is affected by the genetic background, i.e. the mouse strain. To elucidate the mechanism by which cataracts form in the 129Sv/Jae strain earlier than in the C57BL/6J strain, global gene expression was quantitated in the lenses of these strains. Lens cDNAs were analyzed by hybridization to DNA microarrays and with real time-PCR. Theories are proposed based on the observed higher level of expression of the stress-response genes in the C57BL/6J strain and variations in the expression levels of genes involved in protein synthesis, metabolism, catabolism and cell proliferation. How these variations in gene expression might affect the response of lens fiber cells to the increased calcium, caused by lack of alpha3Cx46, is considered. The possibility that the proteins coded by the strain-variable genes might influence the cataract-associated proteolysis of gamma-crystallin is also addressed.
Publication Title
Global gene expression analysis of lenses from different mouse strains and in the alpha3Cx46 knockout mouse.
Sample Metadata Fields
Sex, Age, Specimen part
View Samples- Mus musculus
- 12 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
In order to characterize gene expression networks linked to AT1 angiotensin receptors in the kidney, we carried out genome-wide transcriptional analysis of RNA from kidneys of wild-type (WT) and AT1A receptor-deficient mice (KOs) at baseline and after 2 days of angiotensin II infusion (1 ug/kg/min), using Affymetrix GeneChip Mouse Genome 430 2.0 Arrays. At baseline, 405 genes were differentially expressed (>1.5X) between WT and KO kidneys. Of these, more than 80% were up-regulated in the KO group including genes involved in inflammation, oxidative stress, and cell proliferation. After 2 days of angiotensin II infusion in WT mice, expression of ~805 genes was altered (18% up-regulated, 82% repressed). Genes in metabolism and ion transport pathways were up-regulated while there was attenuated expression of protective genes against oxidative stress including glutathione synthetase and mitochondrial SOD2. Angiotensin II infusion has little effect on blood pressure in KOs. Nonetheless, expression of more than 250 genes was altered in kidneys from KO mice during angiotensin II infusion; 14% were up-regulated, while 86% were repressed including genes involved in immune responses, angiogenesis, and glutathione metabolism. Between WT and KO kidneys during angiotensin II infusion, 728 genes were differentially expressed; 10% were increased and 90% were decreased in the WT group. Differentially regulated pathways included those involved in ion transport, immune responses, metabolism, apoptosis, cell proliferation, and oxidative stress. This genome-wide assessment should facilitate identification of critical distal pathways linked to blood pressure regulation.
Publication Title
Gene expression profiles linked to AT1 angiotensin receptors in the kidney.
Sample Metadata Fields
Sex, Specimen part, Treatment
View Samples