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Links from GEO DataSets

Items: 19

1.

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
2.

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
3.

The Spontaneously Hypertensive Rat: An Experimental Model of Sulfur Dioxide-induced Airways Disease

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is diagnosed by airway obstruction and underlies a group of ailments such as bronchitis, emphysema and often asthma; however, rodent models do not resemble human pathology. Because genetically predisposed spontaneously hypertensive (SH) rats display phenotypes such as systemic inflammation, thrombosis, oxidative stress, and suppressed immune function, that are also apparent in COPD patients, we exposed SH and commonly used male Sprague Dawley (SD) to 0, 250, or 350 ppm sulfur dioxide (SO2), 5h/d for 4 consecutive days. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Dataset:
GDS2372
Platform:
GPL341
16 Samples
Download data
Series
Accession:
GSE4702
ID:
200004702
4.
Full record GDS2372

Sulfur dioxide-induced airways disease model: lungs

Analysis of lungs of spontaneously hypertensive (SH) animals after exposure to 350 ppm sulfur dioxide 5 hours per day for 4 days. Results provide insight into the molecular and genetic basis of the greater susceptibility of SH animals to sulfur dioxide-induced airways disease.
Organism:
Rattus norvegicus
Type:
Expression profiling by array, count, 2 agent, 2 strain sets
Platform:
GPL341
Series:
GSE4702
16 Samples
Download data
DataSet
Accession:
GDS2372
ID:
2372
5.

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
6.
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
7.

The kinetics of transcriptomic changes induced by cigarette smoke in rat lungs

(Submitter supplied) Gene expression profiling in animal models exposed to cigarette mainstream smoke (CS) shapes up as a promising tool for investigating the molecular mechanisms involved in the onset and development of CS-related disease and may aid in the identification of disease candidate genes. Here we report on differential gene expression in lungs of rats exposed for 2, 7, and 13 weeks to 300 and 600 µg total particulate matter (TPM)/l CS with sacrifice 2, 6, or 20 h after the last exposure. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Dataset:
GDS2188
Platform:
GPL3607
18 Samples
Download data
Series
Accession:
GSE4644
ID:
200004644
8.

Gene expression profiles in lung tissue of rats following exposure to mainstream cigarette smoke

(Submitter supplied) Expression data from rats exposed to cigarette smoke (CS) at three concentrations (sham, 300µgTPM/l and 600µgTPM/l) for 13 weeks (5d/week; 2hrs/day) after three different recovery times (2hrs, 6hrs and 20hrs after last treatment); lung tissue Keywords: recovery time course and dose dependency
Organism:
Rattus norvegicus
Type:
Expression profiling by array
Datasets:
GDS2194 GDS2195
Platforms:
GPL341 GPL342
18 Samples
Download data
Series
Accession:
GSE4516
ID:
200004516
9.
Full record GDS2195

Lung response to cigarette smoke: dose response (RAE230B)

Analysis of lungs of animals exposed to 300 or 600 ug total particulate matter (TPM)/l of cigarette smoke (CS) for 13 weeks and allowed to recover 2, 6, or 20 hours after the last exposure. Results provide insight into mechanisms involved in the onset and development of CS-related diseases.
Organism:
Rattus norvegicus
Type:
Expression profiling by array, count, 2 agent, 3 dose, 3 protocol sets
Platform:
GPL342
Series:
GSE4516
9 Samples
Download data
DataSet
Accession:
GDS2195
ID:
2195
10.
Full record GDS2194

Lung response to cigarette smoke: dose response (RAE230A)

Analysis of lungs of animals exposed to 300 or 600 ug total particulate matter (TPM)/l of cigarette smoke (CS) for 13 weeks and allowed to recover 2, 6, or 20 hours after the last exposure. Results provide insight into mechanisms involved in the onset and development of CS-related diseases.
Organism:
Rattus norvegicus
Type:
Expression profiling by array, count, 2 agent, 3 dose, 3 protocol sets
Platform:
GPL341
Series:
GSE4516
9 Samples
Download data
DataSet
Accession:
GDS2194
ID:
2194
11.
Full record GDS2188

Lung response to cigarette smoke: dose response and time course (PIQOR)

Analysis of lungs of animals exposed to 300 or 600 ug total particulate matter (TPM)/l of cigarette smoke (CS) for up to 13 weeks and allowed to recover 2, 6, or 20 hours after the last exposure. Results provide insight into mechanisms involved in the onset and development of CS-related diseases.
Organism:
Rattus norvegicus
Type:
Expression profiling by array, log2 ratio, 2 dose, 3 protocol, 3 time sets
Platform:
GPL3607
Series:
GSE4644
18 Samples
Download data
DataSet
Accession:
GDS2188
ID:
2188
12.

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
13.

Gene expression after 1 and 5 days of cigarette smoke exposure in mice with chronically inflamed or healthy lungs

(Submitter supplied) These studies tested the hypotheses that smoke induces changes in mRNA profiles that are dependent on sex and the health status of the lung, and that the effects of smoke are different after 1 day compared to 5 days of smoke exposure. The ways in which the lungs modulate their response to cigarette smoke after repeated exposures are important for understanding the toxicology of smoke, for developing biomarkers of chronic smoke exposure, and for understanding the therapeutic potential in regulatory signaling pathways that are beneficial or detrimental to lung health. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL22070
79 Samples
Download data: CEL
Series
Accession:
GSE109776
ID:
200109776
14.

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
15.

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
16.

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
17.
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
18.

Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats

(Submitter supplied) Previous studies have shown that smoking induces oxidative stress and inflammation, known factors that coincide with the development and progression of silicosis. Nevertheless, the precise role of cigarette smoke exposure in silicosis and the underlying mechanisms are not clearly understood. Therefore, the objective of the present study was to determine the effect of smoking, if any, on silica-induced pulmonary response and the underlying mechanisms. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18694
24 Samples
Download data: TXT
Series
Accession:
GSE136945
ID:
200136945
19.

Lung response to crystalline nanocellulose exposure in rats

(Submitter supplied) Crystalline nanocellulose (CNC) is an emerging nanomaterial with multiple commercial and industrial applications. Occupational exposure to CNC during the production and/or use of products containing the nanomaterial potentially resulting in adverse health effects among workers is possible. Therefore, there is an immediate need to determine the toxicity potential of CNC. Rats were exposed to either air or CNC (20 mg/m^3, 6 hours/day, 5 days/week, 14 days) and lung toxicity was determined one day following termination of the exposures. more...
Organism:
Rattus norvegicus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL18694
12 Samples
Download data: CSV
Series
Accession:
GSE150567
ID:
200150567
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