GEO DataSets

(Submitter supplied) Although cigarette smoke (CS) is the primary risk factor for COPD, the underlying molecular mechanisms for the significant variability in developing COPD in response to CS are incompletely understood. We performed lung gene expression profiling of two different wild-type murine strains (C57BL/6J, NZW/LacJ) and two genetic models with mutations in COPD GWAS genes (HHIP, FAM13A) after 6 months of chronic CS exposure and compared the results to human COPD lung tissues. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

109 Samples

Download data: TXT

(Submitter supplied) Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death globally, is influenced by both cigarette smoking and genetic determinants. We have previously identified iron-responsive element binding protein 2 (IRP2) as a candidate COPD susceptibility gene based on genetic association studies, with IRP2 increased in the lungs of COPD patients. Here we demonstrate that mice deficient in IRP2 are protected from cigarette smoke (CS)-induced COPD. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL11154

6 Samples

Download data: TXT

(Submitter supplied) Chronic obstructive pulmonary disease (COPD), the fourth leading cause of death globally, is influenced by both cigarette smoking and genetic determinants. We have previously identified iron-responsive element binding protein 2 (IRP2) as a candidate COPD susceptibility gene based on genetic association studies, with IRP2 increased in the lungs of COPD patients. Here we demonstrate that mice deficient in IRP2 are protected from cigarette smoke (CS)-induced COPD. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL17777

11 Samples

Download data: CEL

(Submitter supplied) We have investigated the effects of cigarette smoke exposure in three different strains of mice. DBA/2 and C57Bl/6J are susceptible to smoke and develop different lung changes in response to chronic exposure, while ICR mice are resistant to smoke and do not develop emphysema. The present study was carried out to determine early changes in the gene expression profile of mice exposed to cigarette smoke with either a susceptible or resistant phenotype. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL81

6 Samples

Download data: CEL, CHP

(Submitter supplied) Gene expression data on wild-type and Rora mutant mice exposed to room air and smoke. The results provide a general insight into the relationship of Rora to known DNA damage response pathways and its role in cigarette smoke-induced airspace enlargement.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL7202

12 Samples

Download data: TXT

(Submitter supplied) Our previous study showed that AKR and C57BL/6 mice to cigarette smoke increased lipopolysaccharide (LPS)- induced increased lung vascular permeability. Viremic AKR mice were more susceptible to LPS-induced ALI than C57 on prolonged exposure. In this study we compared the global gene expression patterns to determine the genetic basis for the strain dependent responses to cigarette smoke and LPS-induced ALI. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6246

31 Samples

Download data: CEL, CHP

(Submitter supplied) Multiple gene expression studies have been performed in lung or airway tissues from subjects with chronic obstructive pulmonary disease (COPD). However, in comparison to genome-wide association studies (GWAS), there has been poor replication across these studies. We sought to perform gene expression profiling on a large sample of severe COPD cases and control smokers and use network methods to identify interacting genes and pathways. more...

Organism:

Homo sapiens

Type:

Expression profiling by array

Platform:

GPL10558

151 Samples

Download data: TXT

(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) Cigarette smoke (CS) imposes a strong oxidative burden on exposed tissues resulting in a severely disturbed oxidant/antioxidant balance, which in the context of chronic exposure is assumed to be a key contributor to CS-related diseases. Because of its emerging central role in orchestrating the general cellular antioxidant response, the pathway leading to the activation of the transcription factor Nrf2 has received mounting attention over the past decade in investigations aimed at elucidating CS-induced patho-physiological mechanisms. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3622

Platform:

GPL1261

110 Samples

Download data: CEL

Analysis of lungs from transcription factor Nrf2-deficient animals exposed to cigarette smoke (CS) at various doses and for various lengths of time with or without a subsequent recovery period. Results provide insight into the impact of Nrf2 in acute and subchronic smoking scenarios.

Organism:

Mus musculus

Type:

Expression profiling by array, transformed count, 2 agent, 4 dose, 2 genotype/variation, 3 protocol, 3 time sets

Platform:

GPL1261

Series:

GSE18344

110 Samples

Download data: CEL

(Submitter supplied) Analysis of alveolar macrophage gene expression in C57BL6 wild-type and RAGE null mice exposed to cigarette smoke

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL13112

31 Samples

Download data: XLSX

(Submitter supplied) Transcriptional profiling of lung in mice exposed to cigarette smoke and poly(I:C) and treated or not with Thioredoxin-1

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL5642

1 Sample

Download data: TXT

(Submitter supplied) Purpose: By integrating DNA methylation and gene expression of COPD lung tissues, we identified EPAS1 as a key regulator whose downstream genes significantly overlapped with multiple genes sets associated with COPD disease severity. EPAS1 is distinct in comparison with other key regulators in terms of methylation profiles and downstream target genes. Genes predicted to be regulated by EPAS1 were enriched for biological processes including signaling, cell communications, and system developement. more...

Organism:

Homo sapiens; Mus musculus

Type:

Expression profiling by high throughput sequencing

Platforms:

GPL16791 GPL17021

12 Samples

Download data: TXT

(Submitter supplied) We hypothesize that gene expression in the CS-exposed lungs of this strain (A/J) of mice would be able to give clues about the molecular mechanism of emphysema development, thus contributing to this phenotype. More specifically, although imbalance in oxidants/antioxidants and proteinase/antiproteinase pathways drives the pathogenesis of COPD, the molecular mechanisms involved in the development of emphysema are poorly understood. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Dataset:

GDS3548

Platform:

GPL1261

22 Samples

Download data: CEL, EXP

Analysis of lungs of A/J animals exposed to cigarette smoke (CS) for up to 6 months. A/J animals chronically exposed to CS develop pulmonary emphysema (PE). Results provide insight into the molecular mechanisms underlying the initiation and development of PE.

Organism:

Mus musculus

Type:

Expression profiling by array, count, 2 agent, 4 time sets

Platform:

GPL1261

Series:

GSE8790

22 Samples

Download data: CEL, EXP

(Submitter supplied) We extracted RNA of sorted lung SPC/GFP+ EpCAM+ cells and performed microarray analyses. Total RNA was extracted from sorted Ep-CAMhigh/GFPhigh cells using TRIzol reagent (Invitrogen, Carlsbad, CA) according to the manufacturer’s protocol. The RNA integrity was examined on an Agilent 2100 BioAnalyzer (Agilent Technologies, Santa Clara, CA). Biotinylated ss-cDNA were prepared according to the standard Affymetrix protocol from 100 ng total RNA using the GeneChip WT PLUS Reagent Kit User Manual (Affymetrix/Thermo Fisher Scientific). more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL23038

3 Samples

Download data: CEL

(Submitter supplied) TGFβ inhibition attenuates chronic cigarette smoke induced lung injury and rescues lung architecture.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL8389

20 Samples

Download data: TXT

(Submitter supplied) Increased IGF1 signaling in p16 -/- lungs

Organism:

Mus musculus

Type:

Expression profiling by RT-PCR

Platform:

GPL26852

4 Samples

Download data: XLSX

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is a highly prevalent respiratory disease characterized by airflow limitation and chronic inflammation. MiR-155 is described as an ancient regulator of the immune system. Our objective was to establish a role for miR-155 in cigarette smoke (CS)-induced inflammation and COPD. We demonstrate increased miR-155 expression by RT-qPCR in lung tissue of smokers without airflow limitation and patients with COPD compared to never smokers and in lung tissue and alveolar macrophages of CS-exposed mice compared to air-exposed mice. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL19057

20 Samples

Download data: TXT

(Submitter supplied) BACKGROUND: The HHIP gene, encoding Hedgehog interacting protein, has been implicated in chronic obstructive pulmonary disease (COPD) by genome-wide association studies (GWAS), and our subsequent studies identified a functional upstream genetic variant that decreased HHIP transcription. However, little is known about how HHIP contributes to COPD pathogenesis. METHODS: Here, we exposed Hhip haploinsufficient mice (Hhip+/-) to cigarette smoke (CS) for 6 months to model the biological consequences caused by CS in human COPD risk-allele carriers at the HHIP locus. more...

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL6885

24 Samples

Download data: TXT