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Links from GEO DataSets

Items: 20

1.

Transcriptomic analysis of lung tissue from cigarette smoke induced emphysema murine models and human COPD show shared and distinct pathways

(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
Series
Accession:
GSE87292
ID:
200087292
2.

Irp2 mediates cigarette smoke-induced bronchitis and emphysema via regulation of cytochrome c oxidase and mitochondrial iron loading

(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
Series
Accession:
GSE57073
ID:
200057073
3.

Irp2 mediates cigarette smoke-induced bronchitis and emphysema via regulation of cytochrome c oxidase and mitochondrial iron loading.

(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
Series
Accession:
GSE57048
ID:
200057048
4.

Gene expression data on lungs of wild-type and Rora (Retinoic acid related orphan receptor) mutant mice exposed to room air and smoke

(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
Series
Accession:
GSE33512
ID:
200033512
5.

mouse lung resistance or sensitivity to cigarette smoke

(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
Series
Accession:
GSE12036
ID:
200012036
6.

Murine lung exposed to cigarette smoke and poly(I:C): Thioredoxin-1 vs. Saline Treated

(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
Series
Accession:
GSE49450
ID:
200049450
7.

Functional interactors of genomewide association study genes are differentially expressed in severe chronic obstructive pulmonary disease lung tissue

(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
Series
Accession:
GSE76925
ID:
200076925
8.

Comparative analysis of gene expression in A/J CS vs Air lungs.

(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
Series
Accession:
GSE8790
ID:
200008790
9.
Full record GDS3548

Cigarette smoke-induced pulmonary emphysema model

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
10.

Angiotensin receptor blockade attenuates cigarette smoke-induced lung injury and rescues lung architecture in a murine model

(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
Series
Accession:
GSE33561
ID:
200033561
11.

Integration of RNA-seq transcriptomics with metabolomics in mouse model of cigarette smoke exposure

(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
Series
Accession:
GSE76205
ID:
200076205
12.

The Transcriptome of Nrf2-Deficient Mice in Cigarette Smoke-Induced Emphysematous Changes

(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
Series
Accession:
GSE18344
ID:
200018344
13.
Full record GDS3622

Nrf2-deficient lung response to cigarette smoke: dose response and time course

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
DataSet
Accession:
GDS3622
ID:
3622
14.

Rage null mice exposed to cigarette smoke demonstrate attenuated inflammatory, oxidative and ER stress responses in alveolar macrophages

(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
Series
Accession:
GSE75513
ID:
200075513
15.

Haploinsufficiency of Hedgehog interacting protein causes increased emphysema induced by cigarette smoke through network rewiring

(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
Series
Accession:
GSE65124
ID:
200065124
16.

RNA sequencing (RNA-SEQ) of EPAS1 knockdown by siRNA in endothelial cells

(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
Series
Accession:
GSE62974
ID:
200062974
17.

Targeting p16-induced Senescence Prevents Cigarette Smoke-Induced Emphysema by Promoting IGF1/Akt1 Signaling in mice

(Submitter supplied) Increased IGF1 signaling in p16 -/- lungs
Organism:
Mus musculus
Type:
Expression profiling by RT-PCR
Platform:
GPL26852
4 Samples
Download data: XLSX
Series
Accession:
GSE133380
ID:
200133380
18.

polyA+ RNA sequencing on FACS sorted alveolar macrophages (CD45+SiglecF+CD11c+) from air and cigarette-smoke exposed wild type and miR-155 KO mice

(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
Series
Accession:
GSE137653
ID:
200137653
19.

Chronic rat exposure to cigarette smoke

(Submitter supplied) Chronic obstructive pulmonary disease is a smoking-related disease that lacks effective therapies due partly to the poor understanding of disease pathogenesis. The aim of this study was to identify molecular pathways which could be responsible for the damaging consequences of smoking. To do this, we employed recently described bioinformatic methods to analyze differences in global gene expression, which we then related to the pathological changes induced by cigarette smoke (CS). more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Platform:
GPL85
209 Samples
Download data: CEL
Series
Accession:
GSE7079
ID:
200007079
20.

VD3-VDR axis regulates the homeostasis and function of alveolar macrophage

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing
Platform:
GPL13112
21 Samples
Download data: BEDGRAPH
Series
Accession:
GSE124725
ID:
200124725
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