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Links from GEO DataSets

Items: 20

1.

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
2.

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
3.

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
4.

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
5.
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
6.
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
7.

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
8.

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
9.

Epithelial Expression of Toll-like Receptor 5 is Modulated in Healthy Smokers and Smokers with Chronic Obstructive Lung Disease

(Submitter supplied) The toll-like receptors (TLRs) are important components of the respiratory epithelium host innate defense, enabling the airway surface to recognize and respond to a variety of insults in inhaled air. Based on the knowledge that smokers are more susceptible to pulmonary infection and the airway epithelium of smokers with chronic obstructive pulmonary disease (COPD) is characterized by bacterial colonization and acute exacerbation of airway infections, we assessed whether smoking alters the expression of TLRs in human small airway epithelium, the primary site of smoking-induced disease. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
169 Samples
Download data: CEL, CHP
Series
Accession:
GSE30063
ID:
200030063
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.

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
12.

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
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.

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
15.

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
16.

Human Large Airway Epithelial Cells from healthy never and current smoker and smokers with and without lung cancer

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Homo sapiens
Type:
Expression profiling by array; Expression profiling by high throughput sequencing
Platforms:
GPL13447 GPL10999
21 Samples
Download data: BEDGRAPH, CEL, TXT
Series
Accession:
GSE29007
ID:
200029007
17.

mRNA-seq of Human Airway Epithelial Cells

(Submitter supplied) mRNA expression was profiled from pooled bronchial airway epithelial cell brushings (n=3 patients/pool) obtained during bronchoscopy from healthy never (NS) and current smokers (S) and smokers with (C) and without (NC) lung cancer
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL10999
8 Samples
Download data: BEDGRAPH, GTF, TXT
Series
Accession:
GSE29006
ID:
200029006
18.

Large airway epithelial cells from cigarette smokers with and without lung cancer undergoing flexible bronchoscopy in the operating room for resection of a suspicious lung nodule

(Submitter supplied) mRNA expression was assayed from bronchial epithelial cell samples from smokers with and without lung cancer. A subset of the samples (2 of the lung cancer samples and 3 of the no cancer samples) were pooled and underwent whole transcriptome sequencing. The goals were to compare whole transcriptome sequencing gene expression levels to gene expression levels derived from these samples run on the Affymetrix HGU133A 2.0 platform.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL13447
13 Samples
Download data: CEL
Series
Accession:
GSE28835
ID:
200028835
19.

Persistence of Smoking-induced Dysregulation of Small Airway Epithelium miRNA Expression Despite Smoking Cessation

(Submitter supplied) Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. more...
Organism:
synthetic construct; Homo sapiens
Type:
Non-coding RNA profiling by array
Platform:
GPL14613
29 Samples
Download data: CEL
Series
Accession:
GSE53519
ID:
200053519
20.

Genome-wide analysis reveals mucociliary remodeling of the airway epithelium induced by PM2.5

(Submitter supplied) Air pollution particulate matter <2.5 microns (PM2.5) is associated with poor respiratory outcomes. Mechanisms underlying PM2.5-induced lung pathobiology are poorly understood, but likely involve cellular and molecular changes to the airway epithelium. We extracted and chemically characterized the organic and water-soluble components of contemporary ambient air pollution PM2.5 samples. We then determined the whole transcriptome responses of human mucociliary airway epithelial cultures (n=12) to a dose series  of PM2.5 extracts. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24676
42 Samples
Download data: TXT
Series
Accession:
GSE144770
ID:
200144770
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