GEO DataSets

(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) This study was performed to test the hypothesis that cigarette smoke extract would alter the responses of primary cultures of human bronchial epithelial cells to infection with purified human rhinovirus 16. The data show marked alterations in rhinovirus-induced expression profiles of a number of genes in the presence of cigarette smoke extract (CSE).

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS4832

Platform:

GPL570

16 Samples

Download data: CEL, CHP

Analysis of cultured bronchial epithelial cells (BECs) after rhinovirus (RV) infection, cigarette smoke extract exposure, or both. The airway epithelial cell is the primary site of RV infection. Results provide insight into the impact of cigarette smoking on the response of BECs to RV infections.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 4 agent, 4 individual sets

Platform:

GPL570

Series:

GSE27973

16 Samples

Download data: CEL, CHP

(Submitter supplied) RNA was isolated from bronchial brushings obtained from current and former smokers with and without COPD. mRNA expression was profiled using Affymetrix Human Gene 1.0 ST Arrays.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL13243

269 Samples

Download data: CEL

(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

(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

(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

(Submitter supplied) Cigarette smoke (CS) is the leading cause to develop COPD. Therefore, we investigated the pathologic effects of whole CS on the differentiation of primary small airway epithelial cells (SAEC), from three healthy donors and three COPD patients, cultured under ALI (air-liquid interface) conditions. The analysis of the epithelial physiology demonstrated that CS impaired barrier formation and reduced cilia beat activity. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21290

36 Samples

Download data: TXT

(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

(Submitter supplied) Comparison of gene and protein expression in the large airway epithelium of never and current smokers. Keywords: gene expression array-based (RNA / in situ oligonucleotide)

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL96

8 Samples

Download data: CEL

(Submitter supplied) Chronic obstructive pulmonary disease (COPD), a leading cause of morbidity and mortality, is primarily caused by prolonged exposures to cigarette smoke (CS) and the disease may persist or progress even after smoking cessation. To provide novel insight the mechanisms of COPD development we investigated temporal patterns of lung transcriptome expression in response to chronic CS exposure that also persist following CS cessation, using next generation sequencing techniques. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

62 Samples

Download data: CSV, TXT

(Submitter supplied) The apical junctional complex (AJC), composed of tight junctions and adherens junctions, is essential for maintaining epithelial barrier function. Since cigarette smoking and chronic obstructive pulmonary disease (COPD), the major smoking-induced disease, are both associated with increased lung epithelial permeability, we hypothesized that smoking alters the transcriptional program regulating AJC integrity in the small airway epithelium (SAE), the primary site of pathological changes in COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL570

135 Samples

Download data: CEL, CHP

(Submitter supplied) To investigate the effect of cigarette smoke exposure on gene expression in airway epithelial cells of Canton S Drosophila melanogaster larvae, we isolated the airways of cigarette smoke exposed larvae and air controls. We then performed gene expression profiling analysis using data obtained from RNA-seq of smoke-exposed males, smoke-exposed females, air-control males and air-control females. For each group 4 biological replicates were prepared, representing 40-50 larval airways.

Organism:

Drosophila melanogaster

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19132

16 Samples

Download data: TSV, XLSX

(Submitter supplied) Using primary human bronchial epithelial cells collected at bronchoscopy, we have perturbed signaling pathways important in regulation of response to tobacco smoke exposure and cancer development: ATM, BCL2, GPX1, NOS2, IKBKB, and SIRT1 Using gene expression profiles generated for each pathway and four independent gene expression datasets, we show that SIRT1 activity is significantly up-regulated in cytologically normal airway epithelial cells from active smokers compared to non-smokers; and in contrast, this activity is strikingly down-regulated in non-small cell lung cancer.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10200

52 Samples

Download data: CEL

(Submitter supplied) A number of studies have shown that cigarette smoking produces a field defect, such that genetic mutations induced by smoking occur throughout the lung and its intra and extra-pulmonary airways. Based on this concept, we have begun this study, which has as its goal the definition of the normal airway transcriptome, an analysis of how that transcriptome is affected by cigarette smoke, and to explore the reversibility of altered gene expression when smoking has been discontinued. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Dataset:

GDS534

Platform:

GPL96

75 Samples

Download data: CEL

Analysis of cigarette smoking-induced changes in bronchial epithelia, and reversibility of effects when smoking is discontinued. May provide insight to molecular events leading to chronic obstructive pulmonary disease (COPD) and lung cancer.

Organism:

Homo sapiens

Type:

Expression profiling by array, count, 3 other sets

Platform:

GPL96

Series:

GSE994

75 Samples

Download data: CEL

(Submitter supplied) Our study discusses the importance of studying sex-specific differences in the response of the airway epithelium to chronic injury. It focuses on tracheal epithelial cells from male and female mice exposed to chronic cigarette smoke and found evidence of sex-specific differences in gene expression and epithelial plasticity. Understanding these differences could lead to more effective personalized treatments for respiratory diseases.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

24 Samples

Download data: CSV, GTF

(Submitter supplied) Cigarette smoke (CS) is one of risk factor to chronic obstructive pulmonary disease that is the major causes of death in the world. Furthermore, CS is an independent risk factor for chronic kidney disease (CKD) in the general adult population. The goal of this project was to identified the mechanisms of renal damage that might be associated with exposure to CS extract (CSE) in human kidney proximal tubular epithelial cell line (HK-2 cells) cells.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24676

6 Samples

Download data: TXT

(Submitter supplied) mRNA expression was assayed from bronchial epithelial cells collected via bronchoscopy and nasal epithelial cells collected by brushing the inferior turbinate from healthy current and never smoker volunteers in order to determine the relationship between smoking-related gene expression changes in bronchial and nasal epithelium within the same individual.

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL5175

73 Samples

Download data: CEL

(Submitter supplied) BACKGROUND: We have previously reported gene expression changes in the bronchial airway epithelium of active chronic smokers. In this study, we investigate the effects of Acute Smoke Exposure (ASE) from cigarettes on airway epithelial gene expression. METHODS: Bronchial airway epithelial cell brushings were collected via fiberoptic bronchoscopy from 63 individuals without recent exposure to cigarette smoke (> 2 days), at baseline and at 24 hours after smoking three cigarettes. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL17244

126 Samples

Download data: CEL