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GSE32285
Homo sapiens
8 Downloadable Samples
Illumina HumanRef-8 v3.0 expression beadchip
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Homo sapiens
- 8 Downloadable Samples
Illumina HumanRef-8 v3.0 expression beadchip
Description
The goal of this study was to determine what genes are up- and down-regulated in response to lupus immune complexes in purified CD14+ monocyte stimulations. Our results have shown that novel genes are induced by immune complexes but the response is less robust when using purified monocytes versus total PBMCs
Publication Title
Plasmacytoid dendritic cells and C1q differentially regulate inflammatory gene induction by lupus immune complexes.
Sample Metadata Fields
Specimen part, Treatment, Subject
View Samples- Rattus norvegicus
- 10 Downloadable Samples
- Affymetrix Rat Expression 230A Array (rae230a)
Description
Gene expression analysis in control and diabetic rats. Diabetes-induced erectile dysfunction in rat model of DM. 10 weeks of streptozotocin induced diabetes. F344 Rats.
Publication Title
Microarray analysis reveals novel gene expression changes associated with erectile dysfunction in diabetic rats.
Sample Metadata Fields
No sample metadata fields
View Samples- Arabidopsis thaliana
- 6 Downloadable Samples
- Affymetrix Arabidopsis ATH1 Genome Array (ath1121501)
Description
Transcript profiling and gene expression studies in NAE-treated seedlings: Seeds were germinated and seedlings maintained for 4 d in liquid MS media supplemented with 35 uM NAE(12:0)(N-lauroylethanolamine) prior to RNA isolation.
Publication Title
N-Acylethanolamine metabolism interacts with abscisic acid signaling in Arabidopsis thaliana seedlings.
Sample Metadata Fields
Age, Specimen part, Compound
View Samples- Homo sapiens
- 505 Downloadable Samples
- Affymetrix Human Gene 1.0 ST Array (hugene10st)
Description
We previously derived and validated a bronchial epithelial gene expression biomarker to detect lung cancer in current and former smokers. Given that bronchial and nasal epithelium gene expression is similarly altered by cigarette smoke exposure, we sought to determine if cancer-associated gene expression might also be detectable in more readily accessible nasal epithelium. Nasal epithelial brushings were prospectively collected from current and former smokers with pulmonary lesions suspicious for lung cancer in the AEGIS-1 (n=375) and AEGIS-2 (n=130) clinical trials and gene expression profiled using microarrays. Using the 375 AEGIS 1 samples, we identified 535 genes that were differentially expressed in the nasal epithelium of patients who were ultimately diagnosed with lung cancer vs. those with benign disease after one year of follow-up (p<0.001). Using bronchial gene expression data from 299 AEGIS-1 patients (including 157 patients with matched nasal and bronchial expression data), we found significantly concordant cancer-associated gene expression differences between the two airway sites (p<0.001). Differentially expressed genes were enriched for genes associated with the regulation of apoptosis, mitotic cell cycle, and immune system signaling. A nasal lung cancer classifier derived in the AEGIS-1 cohort that combined clinical factors and nasal gene expression had significantly higher AUC (0.80) and sensitivity (0.94) over a clinical-factor only model (p<0.05) in independent samples from the AEGIS-2 cohort (n=130). These results suggest that the airway epithelial field of lung cancer-associated injury in current and former smokers extends to the nose and demonstrates the potential of using nasal gene expression as a non-invasive biomarker for the detection of lung cancer.
Publication Title
Shared Gene Expression Alterations in Nasal and Bronchial Epithelium for Lung Cancer Detection.
Sample Metadata Fields
Sex, Age
View Samples- Mus musculus
- 9 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Coinhibitory receptor blockade is a promising strategy to boost immunity against a variety of human cancers. However, many patients still do not benefit from this treatment, and responders often experience immune-related toxicities. These issues highlight the need for improved understanding of checkpoint blockade, but the T cell-intrinsic signaling pathways and gene expression profiles engaged during treatment are not well defined, particularly for combination approaches. We utilized a murine model of CD8+ T cell tolerance to address these issues.
Publication Title
Checkpoint blockade immunotherapy relies on T-bet but not Eomes to induce effector function in tumor-infiltrating CD8+ T cells.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 165 Downloadable Samples
- Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Microarray technology provides a powerful tool for defining gene expression profiles of airway epithelium that lend insight into the pathogenesis of human airway disorders. The focus of this study was to establish rigorous quality control parameters to ensure that microarray assessment of the airway epithelium is not confounded by experimental artifact. Samples (total n=223) of trachea, large and small airway epithelium were collected by fiberoptic bronchoscopy of 144 individuals (42 healthy non-smokers, 49 healthy smokers, 11 symptomatic smokers, 22 smokers with lone emphysema with normal spirometry, and 20 smokers with COPD) were processed and hybridized to Affymetrix HG-U133 2.0 Plus microarrays. The pre- and post-chip quality control (QC) criteria established, included: (1) RNA quality, assessed by RNA Integrity Number (RIN) 7.0 using Agilent 2100 Bioanalyzer software; (2) cRNA transcript integrity, assessed by signal intensity ratio of GAPDH 3' to 5' probe sets 3.0; and (3) the multi-chip normalization scaling factor 10.0
Publication Title
Quality control in microarray assessment of gene expression in human airway epithelium.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 118 Downloadable Samples
- Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. Transcriptome analysis revealed a global down-regulation of physiological AJC gene expression in the SAE of healthy smokers (n=53) compared to healthy nonsmokers (n=59), an observation associated with changes in molecular pathways regulating epithelial differentiation such as PTEN signaling and accompanied by induction of cancer-related AJC genes. Genome-wide co-expression analysis identified a smoking-sensitive AJC transcriptional network. The overall expression of AJC-associated genes was further decreased in COPD smokers (n=23). Exposure of human airway epithelial cells to cigarette smoke extract in vitro resulted in down-regulation of several AJC-related genes, accompanied by decreased transepithelial resistance. Thus, cigarette smoking alters the AJC gene expression architecture in the human airway epithelium, providing a molecular basis for the dysregulation of airway epithelial barrier function during the development of smoking-induced lung disease.
Publication Title
Cigarette smoking reprograms apical junctional complex molecular architecture in the human airway epithelium in vivo.
Sample Metadata Fields
Sex, Age
View Samples- Homo sapiens
- 85 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The initial site of smoking-induced lung disease is the small airway epithelium, which is difficult and time consuming to sample by fiberoptic bronchoscopy. We developed a rapid, office-based procedure to obtain trachea epithelium without conscious sedation from healthy nonsmokers (n=26) and healthy smokers (n=19, 27 15 pack-yr). Gene expression differences [fold-change >1.5, p< 0.01, Benjamini-Hochberg correction] were assessed with Affymetrix microarrays. 1,057 probe sets were differentially expressed in healthy smokers vs nonsmokers, representing >500 genes. Trachea gene expression was compared to an independent group of small airway epithelial samples (n=23 healthy nonsmokers, n=19 healthy smokers, 25 12 pack-yr). The trachea epithelium is more sensitive to smoking, responding with 3-fold more differentially-expressed genes than small airway epithelium. The trachea transcriptome paralleled the small airway epithelium, with 156 of 167 (93%) genes that are significantly up- and down-regulated by smoking in the small airway epithelium showing similar direction and magnitude of response to smoking in the trachea. Trachea epithelium can be obtained without conscious sedation, representing a less invasive surrogate canary for smoking-induced changes in the small airway epithelium. This should prove useful in epidemiologic studies correlating gene expression with clinical outcome in assessing smoking-induced lung disease.
Publication Title
Trachea epithelium as a "canary" for cigarette smoking-induced biologic phenotype of the small airway epithelium.
Sample Metadata Fields
Sex, Age
View Samples- Rattus norvegicus
- 10 Downloadable Samples
- Affymetrix Rat Gene 1.0 ST Array (ragene10st)
Description
Different inbred strains of rats differ in their susceptibility to OIR, an animal model of human retinopathy of prematurity. We examined gene expression profiles in Fischer 344 (F344, resistant to OIR) and Sprague Dawley (SD, susceptible to OIR) rats at the early time point of day 3 to identifying gene pathways related to the underlying genetic cause of phenotypic differences between strains.
Publication Title
Gene expression microarray analysis of early oxygen-induced retinopathy in the rat.
Sample Metadata Fields
No sample metadata fields
View Samples