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Links from GEO DataSets

Items: 20

1.
Full record GDS1436

Cigarette smoking effect on alveolar macrophages

Anlaysis of alveolar macrophages of 5 phenotypically normal smokers who consume ~20 packs cigarettes/year. Smoking is the leading cause of respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). Provides insight into early events in molecular pathogenesis of COPD.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 stress sets
Platform:
GPL80
Series:
GSE3212
10 Samples
Download data: CEL, EXP
DataSet
Accession:
GDS1436
ID:
1436
2.

Gene expression in alveolar macrophages from phenotypically normal smokers compared to non-smokers

(Submitter supplied) Cigarette smoking is the leading cause of the respiratory diseases collectively known as chronic obstructive pulmonary disease (COPD). While the pathogenesis of COPD is complex, there is abundant evidence that alveolar macrophages (AM) play an important role. Based on the concept that COPD is a slow-progressing disorder likely involving multiple mediators released by AM activated by cigarette smoke, the present study focuses on the identification of previously unrecognized genes that may be linked to early events in the molecular pathogenesis of COPD, as opposed to factors associated with the presence of disease. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1436
Platform:
GPL80
10 Samples
Download data: CEL, EXP
Series
Accession:
GSE3212
ID:
200003212
3.

Smoking-dependent Reprogramming of Alveolar Macrophage Polarization: Implication for Pathogenesis of COPD

(Submitter supplied) Background: When exposed to specific stimuli, macrophages exhibit distinct activation programs, M1 and M2 polarization, that define macrophage function as inflammatory/immune effectors or anti-inflammatory/tissue remodeling cells, respectively. Due to their position on the lung epithelial surface, alveolar macrophages (AM) directly interact with environmental stimuli such as cigarette smoke, the major risk factor for the development of chronic obstructive pulmonary disease (COPD). more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL570
70 Samples
Download data: CEL, CHP
Series
Accession:
GSE13896
ID:
200013896
4.

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
5.

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
6.
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
7.
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
8.

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
9.

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
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.

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
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.

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
14.

Cigarette smoking alters mRNA expression in human alveolar macrophages

(Submitter supplied) Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
8 Samples
Download data: CEL
Series
Accession:
GSE34517
ID:
200034517
15.

A Distinctive Alveolar Macrophage Activation State Induced by Cigarette Smoking

(Submitter supplied) This series represents alveolar macrophages from a mouse model of emphysema, deletion of the integrin beta6 Keywords: parallel sample
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS1874
Platform:
GPL1792
15 Samples
Download data: TIFF
Series
Accession:
GSE2255
ID:
200002255
16.

isolated alveolar macrophages

(Submitter supplied) This series represents isolated alveolar macrophages from human subjects. Keywords: parallel sample
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS1269
Platform:
GPL570
45 Samples
Download data: CEL
Series
Accession:
GSE2125
ID:
200002125
17.
Full record GDS1874

Integrin beta-6 deficiency model of emphysema: alveolar macrophage

Analysis of alveolar macrophages of integrin beta-6 (Itgb6) deficient animals treated with doxycycline. Itgb6 mutants develop emphysema. Effect of TGFbeta transgene induction to suppress the effect of the Itgb6 mutation also examined.
Organism:
Mus musculus
Type:
Expression profiling by array, log ratio, 3 genotype/variation sets
Platform:
GPL1792
Series:
GSE2255
15 Samples
Download data: TIFF
18.
Full record GDS1269

Cigarette smoking effect on alveolar macrophage

Analysis of alveolar macrophages from 15 cigarette smokers, 15 non-smokers and 15 asthmatics. Results suggest that alveolar macrophage activation induced by smoking contributes to emphysema.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 3 agent sets
Platform:
GPL570
Series:
GSE2125
45 Samples
Download data: CEL
19.

Overexpression of the Apoptotic Cell Removal Receptor, MERTK, in Alveolar Macrophages of Cigarette Smokers

(Submitter supplied) Mononuclear phagocytes play an important role in the removal of apoptotic cells by expressing cell surface receptors that recognize and remove apoptotic cells. Based on the knowledge that cigarette smoking is associated with increased lung cell turnover, we hypothesized that alveolar macrophages (AM) of normal cigarette smokers may exhibit enhanced expression of apoptotic cell removal receptor genes. more...
Organism:
Homo sapiens
Type:
Expression profiling by array
Dataset:
GDS3496
Platform:
GPL570
24 Samples
Download data: CEL, CHP
Series
Accession:
GSE8823
ID:
200008823
20.
Full record GDS3496

Alveolar macrophages of cigarette smokers

Analysis of alveolar macrophages from cigarette smokers. Cigarette smoking is associated with increased lung cell turnover. Mononuclear phagocytes, such as macrophages, play an important role in the removal of apoptotic cells.
Organism:
Homo sapiens
Type:
Expression profiling by array, count, 2 other sets
Platform:
GPL570
Series:
GSE8823
24 Samples
Download data: CEL, CHP
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