GEO DataSets

(Submitter supplied) Enhanced autophagy is recognized as a component of the pathogenesis of smoking-induced airway disease. Based on the knowledge that enhanced autophagy is linked to oxidative stress and the DNA damage response, both of which are linked to smoking, we used microarray analysis of the small airway epithelium to identify smoking up-regulated genes known to re-spond to oxidative stress and the DNA damage response. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

217 Samples

Download data: CEL, CHP

(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:

GPL11154 GPL570

234 Samples

Download data: CEL, CHP, FPKM_TRACKING

(Submitter supplied) Enhanced autophagy is recognized as a component of the pathogenesis of smoking-induced airway disease. Based on the knowledge that enhanced autophagy is linked to oxidative stress and the DNA damage response, both of which are linked to smoking, we used microarray analysis of the small airway epithelium to identify smoking up-regulated genes known to re-spond to oxidative stress and the DNA damage response. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

17 Samples

Download data: FPKM_TRACKING

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing; Expression profiling by array

Platforms:

GPL11154 GPL570

193 Samples

Download data: CEL, CHP, FPKM_TRACKING

(Submitter supplied) In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU2AF1, a known transcription co-factor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of up-regulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation and analysis of differentiating single basal cell clones. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

184 Samples

Download data: CEL, CHP

(Submitter supplied) In the process of seeking novel lung host defense regulators by analyzing genome-wide RNA sequence data from normal human airway epithelium, we detected expression of POU2AF1, a known transcription co-factor previously thought to be expressed only in lymphocytes. Lymphocyte contamination of human airway epithelial samples obtained by bronchoscopy and brushing was excluded by immunohistochemistry staining, the observation of up-regulation of POU2AF1 in purified airway basal stem/progenitor cells undergoing differentiation and analysis of differentiating single basal cell clones. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

9 Samples

Download data: FPKM_TRACKING

(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

(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

(Submitter supplied) Epigenetic factors and related small molecules have emerged to be strongly involved in autophagy process. Here we report that two inhibitors of histone H3K4 demethylase KDM1A/LSD1, 2-PCPA and GSK-LSD1, are able to induce autophagy in multiple cell lines. The two small molecules induced accumulation of LC3II, formation of autophagosome, fusion of autophagosome with lysosome and SQSTM1/p62 degradation. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL16791

14 Samples

Download data: TXT

(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

(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

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

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

(Submitter supplied) To investigate the biochemical and genetic alterations that occur in response to cigarette smoke exposure among airway epithelial cells from different sites in the lungs, we performed microarray-based analysis using small airway epithelial cells (SAEC) and normal human bronchial epithelial cells (NHBE) following 24 h of cigarette smoke extract (CSE). In microarray-based analysis, the small airway showed higher susceptibility to CS compared to the large airway, such as enhanced expression of inflammatory-related pathways including the TNF signaling pathway. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL4133

8 Samples

Download data: TXT

(Submitter supplied) The small airway epithelium (SAE) the pseudostratified epithelium that covers the majority of the human airway surface from the 6th generation to the alveoli, is the major site of lung disease caused by smoking, and the cell population that exhibits the earliest manifestations of smoking-induced disease. The focus of this study is to use RNA-Seq (massive parallel sequencing technology) to sequence all polyA+ mRNAs expressed by the SAE of healthy nonsmokers to gain new insights into the biology of the SAE, and how these cells respond to cigarette smoke. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

27 Samples

Download data: CEL, CHP

(Submitter supplied) Although smoking-induced lung disease tends to be more common in the upper lobe, it is not known if this results from the skewed distribution of inhaled cigarette smoke or increased susceptibility of the upper lobes to these disorders. The distribution of inhaled cigarette smoke within the lung is complex, depending on lung pressure-volume relationships, gravity, individual smoking habits and the properties of the individual components of cigarette smoke. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

22 Samples

Download data: CEL, CHP