Filters
Technology
Platform
SRP072571
Rattus norvegicus
15 Downloadable Samples
Illumina HiSeq 1000
Description
Zinc is both an essential and potentially toxic metal. It is widely believed that oral zinc supplementation can reduce the effects of the common cold; however, there is strong clinical evidence that intranasal (IN) zinc gluconate (ZG) gel treatment for this purpose causes anosmia, or the loss of the sense of smell, in humans. Using the rat olfactory neuron cell line, Odora, we investigated the molecular mechanism by which zinc exposure exerts its toxic effects on olfactory neurons. Following treatment of Odora cells with 100 and 200 µM ZG for 0-24 h, RNA-seq and in silico analyses revealed up-regulation of pathways associated with zinc metal response, oxidative stress, and ATP production. We observed that Odora cells recovered from zinc-induced oxidative stress, but ATP depletion persisted with longer exposure to ZG. ZG exposure increased levels of NLRP3 and IL-1ß protein levels in a time-dependent manner, suggesting that zinc exposure may cause an inflammasome-mediated cell death, pyroptosis, in olfactory neurons. Overall design: 5 treatment groups, 3 replicates/group, 1 control group, 3 groups treated with 100 µM zinc gluconate for increasing time (6, 12, and 24 h), 1 group treated with 200 µM zinc gluconate for 6 h
Publication Title
Mechanistic studies of the toxicity of zinc gluconate in the olfactory neuronal cell line Odora.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 23 Downloadable Samples
Affymetrix Human Genome U95 Version 2 Array (hgu95av2)
Description
Rotavirus infection is the single most important cause of severe diarrhea in young children worldwide. We used Affymetrix Human U95Av2 high density oligonucleotide arrays to compare gene expression profiles in peripheral blood mononuclear cells (PBMC) of 10 children with acute rotavirus diarrhea and 8 age-matched healthy children. We also examined patterns of gene expression in 5 convalescent-phase PBMC samples from rotavirus patients. For data analysis, we imported .cel files generated by Affymetrix MAS5.0 into Genetraffic 3.1 software (Iobion) and performed robust multi-chip analysis. We considered a gene in patients differentially expressed if its level of expression was at least 1.5-fold higher or lower than the baseline (arithmetic mean) of the corresponding gene in 8 controls and if its pattern of elevated or repressed expression was observed in at least 7 of the 10 patients. Using these criteria, we identified ~1% up- and ~2% down-regulated genes in acute-phase PBMC of patients. Up-regulated genes included those involved in the differentiation, maturation, activation, and survival of B cells, as well as an array of genes with function in inflammatory and antiviral activities. We observed a pattern of repressed expression of a number of genes involved in the various stages of T-cell development and activation. On the basis of these results, we conclude that rotavirus infection induces robust inflammatory response and B-cell activation but represses T-cell response.
Publication Title
Rotavirus infection alters peripheral T-cell homeostasis in children with acute diarrhea.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 33 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Molecular Aging of Human Liver: An Epigenetic/Transcriptomic Signature.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Homo sapiens
- 33 Downloadable Samples
Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Gene expression profiling of liver biopsies collected from 33 healthy liver donors ranging from 13 to 90 years old. The Affymetrix HG-U133 Plus 2.0 GeneChip platform was used to evaluate gene-expression.
Publication Title
Molecular Aging of Human Liver: An Epigenetic/Transcriptomic Signature.
Sample Metadata Fields
Sex, Age, Specimen part, Disease
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Dendritic cells (DC) are the most potent antigen-presenting cells of the immune system. In lymph nodes (LN), they are also believed to dispose of apoptotic cells, a critical function usually achieved by macrophages (M) in other tissues. We report a population of tolerogenic M located in the T cell zone of LN. T zone M (TZM) are long lived M seeded after birth and slowly replaced by blood monocytes. We show that TZM but not DC act as the only professional scavengers clearing apoptotic cells in the LN T cell zone. Importantly, we demonstrate that TZM prevent the capture of apoptotic cells by DC and the associated potential noxious activation of T cell immunity. We thus propose a new model in which efferocytosis and T cell activation are uncoupled processes handled by TZM and DC respectively.
Publication Title
T Cell Zone Resident Macrophages Silently Dispose of Apoptotic Cells in the Lymph Node.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 36 Downloadable Samples
- Illumina HumanHT-12 V4.0 expression beadchip
Description
Facioscapulohumeral dystrophy (FSHD) is one of the most common inherited muscular dystrophies. The causative gene remains controversial and the mechanism of pathophysiology unknown. Here we identify genes associated with germline and early stem cell development as targets of the DUX4 transcription factor, a leading candidate gene for FSHD. The genes regulated by DUX4 are reliably detected in FSHD muscle but not in controls, providing direct support for the model that misexpression of DUX4 is a causal factor for FSHD. Additionally, we show that DUX4 binds and activates LTR elements from a class of MaLR endogenous primate retrotransposons and suppresses the innate immune response to viral infection, at least in part through the activation of DEFB103, a human defensin that can inhibit muscle differentiation. These findings suggest specific mechanisms of FSHD pathology and identify candidate biomarkers for disease diagnosis and progression.
Publication Title
DUX4 activates germline genes, retroelements, and immune mediators: implications for facioscapulohumeral dystrophy.
Sample Metadata Fields
Specimen part
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Gene 1.0 ST Array (mogene10st)
Description
Murine MafB/c-MAF double KO (Maf-DKO) primary macrophages are known for their unlimited non-tumorigenic self-renewal ability (Aziz et al., 2009). In an in vitro screen for cytokines and small molecules we identified Niacinamide (NAM) a potent inhibitor of their proliferative potential characterized by a reversible cell cycle arrest.
Publication Title
SIRT1 regulates macrophage self-renewal.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 45 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Context: In many cancers, specific subpopulations of cells appear to be uniquely capable of initiating and maintaining tumors. The strongest support for this cancer stem cell model comes from transplantation assays in immune-deficient mice indicating that human acute myeloid leukemia (AML) is organized as a cellular hierarchy driven by self-renewing leukemia stem cells (LSC). This model has significant implications for the development of novel therapies, but its clinical significance remains unclear.
Publication Title
Association of a leukemic stem cell gene expression signature with clinical outcomes in acute myeloid leukemia.
Sample Metadata Fields
Disease, Disease stage, Subject
View Samples- Danio rerio
- 12 Downloadable Samples
- Affymetrix Zebrafish Genome Array (zebrafish)
Description
Purpose: Investigate the molecular determinants of retinal regeneration in adult vertebrates by analyzing the gene expression profiles of control and post-lesion retina of adult zebrafish, a system that regenerates following injury.
Publication Title
Gene expression profiles of intact and regenerating zebrafish retina.
Sample Metadata Fields
No sample metadata fields
View Samples- Homo sapiens
- 98 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Acute Myeloid Leukemia AML is a cancer in which the process of normal cell hematopoietic differentiation is disrupted. Evidence exists that AML comprises a hierarchy with leukemic stem cells giving rise to more differentiated, but immature and functionally incompetent populations. The similarity of these AML subpopulations to normal stages of hematopoietic differentiation has not been dissected comprehensively at the transcriptional level. Here we introduce Normal Memory Analysis (NorMA), a data analysis method that extracts from omic data the remnants of the healthy normal-like phenotype. Applying NorMA to gene expression data from AML uncovered a wealth of information in the normal-like component of data: the normal hematopoietic memory of AML tumor cells. We found significant variation within the patient population, and we found strong association of this normal hematopoietic memory with survival. We found that undifferentiated NorMA phenotype has significantly worse survival than differentiated NorMA phenotype, showing that the NorMA classification of tumors captures a biologically meaningful stratification of patients, with highly significant survival association. Patients with NorMA phenotype in the undifferentiated Hematopoietic Stem Cell HSC stage had the worst survival, with median survival time under 6 months. We further found significant survival differences between tumor groups with differentiated NorMA phenotype, depending on their hematopoietic path: AML patients with NorMA phenotype in megakaryocyte-erythroid progenitor MEP stage had significantly better survival than those with NorMA phenotype in granulocyte-macrophage progenitor GMP stage. Thus NorMA produced a stratification of AML cohorts by differentiation stage, with significant outcome differences. It also provided clean molecular signatures for these stages. NorMA can be used in many other contexts, to explore for example the tumor cell of origin, or disease predisposition.
Publication Title
An LSC epigenetic signature is largely mutation independent and implicates the HOXA cluster in AML pathogenesis.
Sample Metadata Fields
Specimen part
View Samples