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Links from GEO DataSets

Items: 20

1.

Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages

(Submitter supplied) Disparate Oxidant-related Gene Expression of Human Small Airway Epithelium Compared to Autologous Alveolar Macrophages in Response to the In Vivo Oxidant Stress of Cigarette Smoking The oxidant burden of cigarette smoking induces lung cell dysfunction, and play a significant role in the pathogenesis of lung disease. Two cell populations directly exposed to the oxidants in cigarette smoke are the small airway epithelium and alveolar macrophages. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
98 Samples
Download data: CEL, CHP
Series
Accession:
GSE13931
ID:
200013931
2.

Genes Associated with MUC5AC Expression in the Human Airway Epithelium

(Submitter supplied) To help define the genes associated with mucus synthesis and secretion in the human small airway epithelium, we hypothesized that comparison of the transcriptomes of the small airway epithelium of individuals that express high vs low levels of MUC5AC, a major secretory mucin and the major component of airway mucus, could be used as a probe to identify the genes related to human small airway mucus production / secretion. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
132 Samples
Download data: CEL, CHP, TXT
Series
Accession:
GSE34450
ID:
200034450
3.

Coordinate Control of Nrf2 Mediated Genes in the Human Small Airway Epithelium Highly Responsive to Smoking

(Submitter supplied) Nuclear factor erythroid 2-related factor 2 (NFE2L2, Nrf2) is an oxidant responsive transcription factor known to induce phase 2 detoxifying and antioxidant genes to protect cells from oxidative stress. Cigarette smoke, with its large oxidant content, is a major stressor to the small airway epithelium, the cells of which are vulnerable to oxidant damage and consequent malignant transformation. In this study, we assessed the role of cigarette smoke in activation of Nrf2 in the human small airway epithelium in vivo. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
83 Samples
Download data: CEL, CHP
Series
Accession:
GSE11952
ID:
200011952
4.

Down-regulation of the Notch Differentiation Pathway in the Airway Epithelium of Normal Smokers and Smokers with COPD

(Submitter supplied) Down-regulation of the Notch Differentiation Pathway in the Human Airway Epithelium in Normal Smokers and Smokers with Chronic Obstructive Lung Disease In cigarette smokers, the toxic components of smoke place the epithelium under the constant stress of a variety of mechanisms of injury, with consequent modulation of airway epithelial regeneration and disordered differentiation. Based on the underlying hypothesis that these airway epithelial changes must involve quantitative changes in genes involved with the regulation of differentiation, we assessed the expression of the Notch pathway, a signaling pathway known to play a fundamental role in the embryonic lung as a gatekeeper for differentiation, in the small airway epithelium of non-smokers, normal smokers, and smokers with COPD. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
20 Samples
Download data: CEL, CHP
Series
Accession:
GSE7832
ID:
200007832
5.

Airway epithelium, small airways, normal non-smokers, phenotypic normal smokers, smokers with COPD and early COPD

(Submitter supplied) Upregulation of Expression of the Ubiquitin Carboxyl Terminal Hydrolase L1 Gene in Human Airway Epithelium of Cigarette Smokers The microarray data deposited here is from 39 HG-U133 Plus 2.0 GeneChips, from 12 normal non-smokers, 12 phenotypic normal smokers, 9 Early COPD and 6 COPD individuals, all small airways, all small airway. A subset of these samples have been already submitted under GEO Accession Number GSE 4498. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
39 Samples
Download data: CEL, CHP
Series
Accession:
GSE5058
ID:
200005058
6.

Expression data of small airway epithelium from phenotypically normal smokers and non-smokers

(Submitter supplied) Modification of Gene Expression of the Small Airway Epithelium in Response to Cigarette Smoking The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (HG-133 Plus 2.0 array) in phenotypically normal smokers (n=10, 33 ± 7 pack-yr) compared to matched non-smokers (n=12). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS2486
Platform:
GPL570
22 Samples
Download data: CEL, CHP
Series
Accession:
GSE4498
ID:
200004498
7.
Full record GDS2486

Small airway epithelium response to cigarette smoking

Analysis of small airway epithelial cells of phenotypically normal smokers. The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. Results provide insight into how smoking modifies small airway structure and function.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 stress sets
Platform:
GPL570
Series:
GSE4498
22 Samples
Download data: CEL, CHP
8.

Gene expression profile of small airway epithelium of normal non-smokers and normal smokers

(Submitter supplied) The earliest morphologic evidence of changes in the airways associated with chronic cigarette smoking is in the small airways. To help understand how smoking modifies small airway structure and function, we developed a strategy using fiberoptic bronchoscopy and brushing to sample the human small airway (10th-12th order) bronchial epithelium to assess gene expression (Affymetrix HG-U133A array) in phenotypically normal smokers (n=6, 24 ± 4 pack-yr) compared to matched non-smokers (n=5). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1304
Platform:
GPL96
11 Samples
Download data
Series
Accession:
GSE3320
ID:
200003320
9.
Full record GDS1304

Cigarette smoking effect on small airway epithelium

Analysis of phenotypically normal 10th to 12th order small airway bronchial epithelia from cigarette smokers. Cigarette smoking is the most common cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the early pathogenesis of COPD.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 stress sets
Platform:
GPL96
Series:
GSE3320
11 Samples
Download data
DataSet
Accession:
GDS1304
ID:
1304
10.

Variability in Small Airway Epithelial Gene Expression Among Normal Smokers

(Submitter supplied) Despite overwhelming data that cigarette smoking causes chronic obstructive pulmonary disease (COPD), only a minority of chronic smokers are affected, strongly suggesting that genetic factors modify susceptibility to this disease. We hypothesized that there are individual variations in the response to cigarette smoking, with variability among smokers in expression levels of protective / susceptibility genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
54 Samples
Download data: CEL, CHP
Series
Accession:
GSE8545
ID:
200008545
11.

Smoking-induced Wnt pathway downregulation

(Submitter supplied) The Wnt pathway plays a central role in controlling differentiation of epithelial tissues; when Wnt is on, differentiation is suppressed, but when Wnt is off, differentiation is allowed to proceed. Based on this concept, we hypothesized that expression of key genes in the Wnt pathway are suppressed in the human airway epithelium under the stress of cigarette smoking, a stress associated with dysregulation of the differentiated state of the airway epithelium. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
127 Samples
Download data: CEL, CHP
Series
Accession:
GSE19407
ID:
200019407
12.

Smoking-mediated Up-regulation of GAD67 Expression in the Human Airway Epithelium

(Submitter supplied) Gamma-aminobutyric acid (GABA) is a multifunctional mediator that functions as a neurotransmitter in the central nervous system and a trophic factor during nervous system development, affecting proliferation, differentiation and cell death [1-3].GABA is synthesized from glutamate, catalyzed by GAD65 and GAD67, glutamic acid decarboxylase {Tillakaratne, Medina-Kauwe, et al. 1995 21 /id}{Owens & Kriegstein 2002 3 /id}{Watanabe, Maemura, et al. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
157 Samples
Download data: CEL, CHP
Series
Accession:
GSE17905
ID:
200017905
13.

Biologic Phenotyping of the Human Small Airway Epithelial Response to Cigarette Smoking

(Submitter supplied) The first changes associated with smoking are in the small airway epithelium (SAE). Given that smoking alters SAE gene expression, but only a fraction of smokers develop chronic obstructive pulmonary disease (COPD), we hypothesized that assessment of SAE genome-wide gene expression would permit biologic phenotyping of the smoking response, and that a subset of healthy smokers would have a “COPD-like” SAE transcriptome. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
171 Samples
Download data: CEL, CHP
Series
Accession:
GSE11784
ID:
200011784
14.

Expression data from buccal and nasal epithelium of current and never smokers

(Submitter supplied) Smoking is the leading cause of lung cancer death, although only a small percentage of smokers develop the disease. Cigarette smoke exposure is known to cause a field of injury in cells throughout the respiratory tract, and while these airway epithelial cells are morphologically normal, they can undergo genetic alterations in response to cigarette smoke exposure. We used microarrays to analyze the gene expression of epithelial cells in the extrathoracic epithelium, specifically nasal and buccal epithelium, to see if these cells underwent similar genetic alterations in response to tobacco exposure as seen in bronchial epithelial cells as has been previously reported. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Datasets:
GDS3054 GDS3309
Platforms:
GPL96 GPL571
25 Samples
Download data: CEL, CHP, EXP
Series
Accession:
GSE8987
ID:
200008987
15.
Full record GDS3309

Cigarette smoking effect on the nasal epithelium

Analysis of nasal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the nose.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent sets
Platform:
GPL571
Series:
GSE8987
15 Samples
Download data: CEL, CHP, EXP
16.
Full record GDS3054

Cigarette smoking effect on the buccal epithelium

Analysis of buccal epithelia from cigarette smokers. Cigarette smoke creates a field of injury in epithelial cells lining the respiratory tract. Results extend the concept of a smoking-induced field of injury beyond intrathoracic (bronchial) epithelia to extrathoracic epithelia that line the mouth.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 agent sets
Platform:
GPL96
Series:
GSE8987
10 Samples
Download data: CEL, CHP, EXP
17.

Decreased Expression of Intelectin 1 in The Human Airway Epithelium of Smokers Compared to Nonsmokers

(Submitter supplied) Lectins are proteins present on cell surfaces or as shed extracellular proteins that function in innate immune defense as phagocytic receptors to recognize specific bacterial cell wall components. Based on the knowledge that cigarette smoking is associated with increased risk of bacterial infection, we hypothesized that cigarette smoking may modulate the expression of lectin genes in the airway epithelium. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
87 Samples
Download data: CEL, CHP
Series
Accession:
GSE10006
ID:
200010006
18.

Cigarette Smoking Induces Overexpression of a Fat Depleting Gene AZGP1 in the Human Airway Epithelium

(Submitter supplied) Smokers weigh less and have less body fat than non-smokers, and increased body fat and weight gain are observed following smoking cessation. To assess a possible molecular mechanism underlying the inverse association between smoking and body weight, we hypothesized that smoking may induce the expression of a fat depleting gene in the airway epithelium, the cell population that takes the brunt of the stress of cigarette smoke. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platforms:
GPL80 GPL570 GPL96
92 Samples
Download data: CEL, CHP
Series
Accession:
GSE10135
ID:
200010135
19.

Smoking-induced Up-regulation of AKR1B10 Expression in the Airway Epithelium of Healthy Individuals

(Submitter supplied) The aldokatoreductases (AKRs) represent a gene superfamily that code for monomeric, soluble NAD(P)H-dependent oxidoreductases that mediate elimination reactions. AKR1B10, an AKR that functions to eliminate retinals, has been observed to be upregulated in squamous metaplasma and non small cell lung cancer, and has been suggested as a diagnostic marker specific to tobacco-related carcinogenesis. In the context of the link of smoking and lung cancer and the enhanced expression of AKR1B10 expression in lung cancer, we hypothesize that enhanced expression of AKR1B10 may be initiated in healthy smokers, prior to the development of any evidence of lung cancer. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
161 Samples
Download data: CEL, CHP
Series
Accession:
GSE18385
ID:
200018385
20.

Threshold of Biologic Response of the Small Airway Epithelium to Low Levels of Tobacco Smoke

(Submitter supplied) Background: Healthy individuals exposed to low levels of cigarette smoke have a decrement in lung function and higher risk for lung disease compared to unexposed individuals. We hypothesized that healthy individuals exposed to low levels of tobacco smoke must have biologic changes in the small airway epithelium compared to healthy unexposed individuals. Methods: Small airway epithelium was obtained by bronchoscopy from 121 individuals; microarrays assessed genome wide gene expression, and urine nicotine and cotinine were used to categorized subjects as “nonsmokers,” “active smokers,” and “low exposure.” The gene expression data was used to determine the threshold and ID50 of urine nicotine and cotinine at which the small airway epithelium showed abnormal responses. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
121 Samples
Download data: CEL, CHP
Series
Accession:
GSE19667
ID:
200019667
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