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GSE22879
Mus musculus
4 Downloadable Samples
Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Partial hepatectomy, resection of a portion of liver mass, indues significant liver regenerative responses that consist of numerous genetic changes. To identify specific genetic changes, we compare the liver of mice underwent either hepatectomy or sham operation.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 3 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Endothelial cells were transduced with different genes modulating signaling pathways and compared to GFP transduced control group to identify changes in the expression of the angiocrine factors.
Publication Title
No associated publication
Sample Metadata Fields
Specimen part, Treatment
View Samples- Mus musculus
- 2 Downloadable Samples
- Affymetrix Mouse Genome 430 2.0 Array (mouse4302)
Description
Mouse lymphoma cells were co-cultured with endothelial cells in serum/cytokine-free condition. To identify specific genetic changes, we compared lymphoma cells cultured in medium containing 10% fetal bovine serum with lymphoma cells co-cultured with endothelial cells.
Publication Title
Angiocrine factors deployed by tumor vascular niche induce B cell lymphoma invasiveness and chemoresistance.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 399 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Epidemiological studies have demonstrated that exposure to particulate matter (PM) ambient pollution has adverse effects on lung health, exacerbated by cigarette smoking. Fine airborne particles <2.5 m (PM2.5) are the most harmful of the urban pollutants, and the most closely linked to respiratory disease. Based on the knowledge that the small airway epithelium (SAE) plays a central role in pathogenesis of smoking-related lung disease, we hypothesized that elevated PM2.5 levels are associated with dysregulation of SAE gene expression.
Publication Title
Ambient Pollution-related Reprogramming of the Human Small Airway Epithelial Transcriptome.
Sample Metadata Fields
Specimen part
View Samples- Homo sapiens
- 220 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Cystatin A (gene: CSTA), is up-regulated in non-small-cell lung cancer (NSCLC) and dysplastic vs normal human bronchial epithelium. In the context that chronic obstructive pulmonary disease (COPD), a small airway epithelium (SAE) disorder, is independently associated with NSCLC (especially squamous cell carcinoma, SCC), but only occurs in a subset of smokers, we hypothesized that genetic variation, smoking and COPD modulate CSTA gene expression levels in SAE, with further up-regulation in SCC. Gene expression was assessed by microarray in SAE of 178 individuals [healthy nonsmokers (n=60), healthy smokers (n=82), and COPD smokers (n=36)], with corresponding large airway epithelium (LAE) data in a subset (n=52). Blood DNA was genotyped by SNP microarray. Twelve SNPs upstream of the CSTA gene were all significantly associated with CSTA SAE gene expression (p<0.04 to 5 x 10-4). CSTA gene expression levels in SAE were higher in COPD smokers (28.4 2.0) than healthy smokers (19.9 1.4, p<10-3), who in turn had higher levels than nonsmokers (16.1 1.1, p<0.04). CSTA LAE gene expression was also smoking-responsive (p<10-3). Using comparable publicly available NSCLC expression data, CSTA was up-regulated in SCC vs LAE (p<10-2) and down-regulated in adenocarcinoma vs SAE (p<10-7). All phenotypes were associated with significantly different proportional gene expression of CSTA to cathepsins. The data demonstrate that regulation of CSTA expression in human airway epithelium is influenced by genetic variability, smoking, and COPD, and is further up-regulated in SCC, all of which should be taken into account when considering the role of CSTA in NSCLC pathogenesis.
Publication Title
Modulation of cystatin A expression in human airway epithelium related to genotype, smoking, COPD, and lung cancer.
Sample Metadata Fields
Race
View Samples- Homo sapiens
- 187 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
This SuperSeries is composed of the SubSeries listed below.
Publication Title
Role of OSGIN1 in mediating smoking-induced autophagy in the human airway epithelium.
Sample Metadata Fields
Specimen part, Race
View Samples- Homo sapiens
- 120 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Motivation: Identification of eQTL, the genetic loci that contribute to heritable variation in gene expression, can be obstructed by factors that produce variation in expression profiles if these factors are unmeasured or hidden from direct analysis.
Publication Title
HEFT: eQTL analysis of many thousands of expressed genes while simultaneously controlling for hidden factors.
Sample Metadata Fields
Disease, Race
View Samples- Homo sapiens
- 202 Downloadable Samples
- Affymetrix Human Full Length HuGeneFL Array (hu6800), Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
Smoking-induced lung disease is one of the most prevalent forms of lung disease but also one of the more diverse. Based on the phenotypic diversity caused by the same environmental stress, we hypothesized that smoking may induce changes in lung cell expression of genes that, with specific variants, are causative of monogenic lung disease, i.e., not that smoking induces a phenocopy of a genetic disease, but smoking may subtly modify the expression of genes known to be associated with genetic disorders with distinct lung disease phenotypes. To assess this hypothesis, and based on the knowledge that most smoking-related disease phenotypes start in the small airway epithelium, we asked: are the genes associated with the monogenic lung disorders expressed in the small airway epithelium, and if so, does smoking alter the expression of these genes? To accomplish this, we examined small airway epithelium expression of 92 genes known to be associated with 17 monogenic lung disorders in 230 samples of small airway epithelium (SAE) obtained from healthy nonsmokers and healthy smokers without any clinical evidence of disease. Of the 86 monogenic disorder-related genes we found expressed in the SAE, strikingly, 37 were significantly differentially expressed in normal smokers compared to normal nonsmokers (p<0.05, Benjamini-Hochberg correction for multiple comparisons). The data demonstrates that the effect of smoking on the transcriptome of small airway epithelium includes significantly altered regulation of the genes responsible for known monogenic disorders.
Publication Title
Cigarette Smoking Induces Changes in Airway Epithelial Expression of Genes Associated with Monogenic Lung Disorders.
Sample Metadata Fields
Sex, Age, Race
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
- 191 Downloadable Samples
- Affymetrix Human Genome U133 Plus 2.0 Array (hgu133plus2)
Description
The proximal-distal patterning program determines unique structural and functional properties of proximal and distal airways in the adult lung. Based on the knowledge that remod-eling of distal airways is the major pathologic feature of chronic obstructive pulmonary disease (COPD), and that small airway epithelium (SAE), which covers distal airways, is the primary site of the initial smoking-induced changes relevant to COPD pathogenesis, we hypothesized that in COPD smokers, the SAE transcriptome loses its region-specific biologic identity and takes on the transcriptional pattern of the proximal airways. By analyzing human airway epithelium col-lected by bronchoscopic brushings from proximal and distal airways of healthy smokers, proxi-mal and distal airway epithelial transcriptome signatures were identified. Dramatic smoking-dependent suppression of distal signature paralleled by acquisition of the proximal airway epithe-lial phenotype was found in the SAE of COPD smokers. Distal-proximal re-patterning observed in the SAE of smokers in vivo was reproduced in vitro by stimulating SAE basal cells (BC), the stem/progenitor cells of the SAE, with EGF, a growth factor up-regulated in airway epithelium by smoking. Together, this study identifies distal-proximal SAE re-patterning as a characteristic feature of small airway disordering in COPD smokers potentially driven by EGF/EGFR-mediated reprogramming of SAE BC stem/progenitor cells.
Publication Title
Smoking-Dependent Distal-to-Proximal Repatterning of the Adult Human Small Airway Epithelium.
Sample Metadata Fields
Specimen part, Race
View Samples