Similar studies for GEO DataSets (Select 3622) - GEO DataSets

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Items: 20

Select item 36221.

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

Select item 2000183442.

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

Select item 2000046443.

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

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Series

Accession:: GSE4644

ID:: 200004644

Select item 2000045164.

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:: GPL342 GPL341
18 Samples

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Series

Accession:: GSE4516

ID:: 200004516

Select item 21955.

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

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DataSet

Accession:: GDS2195

ID:: 2195

Select item 21946.

Lung response to cigarette smoke: dose response (RAE230A)

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

Select item 21887.

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

Select item 2000087908.

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

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 35489.

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

DataSet

Accession:: GDS3548

ID:: 3548

PubMed Full text in PMC Similar studies GEO Profiles Analyze DataSet

Select item 20008729210.

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

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Select item 20004604811.

High expression genes in urethane-induced lung tumor

(Submitter supplied) We estimated differences of urethane-induced tumors between Nrf2+/+ and Nrf2-/- ICR mouse. To identify Nrf2-regulated genes in tumors, we examined the mRNA expression profile both in tumor and non-tumor tissue of mouse 4 months after urethane administration.

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL4134
4 Samples

Download data: TXT

Series

Accession:: GSE46048

ID:: 200046048

Select item 20010977612.

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

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Select item 20000781013.

Comparative analysis of gene expression WT and Nrf2-/- mice Type II cells

(Submitter supplied) We hypothesize that gene expression in the Type II cells of Nrf2+/+ and Nrf2-/- mice are divergent thus contributing the cell growth. More specifically, type II cells from Nrf2-/- mice have increased reactive oxygen species that cause the impaired cell growth. In order to test these hypotheses at the gene expression level, we utilized microarray analysis to examine transcriptional differences between Nrf2+/+ and Nrf2-/- cells. more...

Organism:: Mus musculus

Type:: Expression profiling by array

Dataset:: GDS2875
Platform:: GPL1261
9 Samples

Download data: CEL

Series

Accession:: GSE7810

ID:: 200007810

Select item 287514.

Nrf2-deficient type II lung epithelial cell response to antioxidant supplementation

Analysis of Nrf2 deficient lung epithelial cells treated with the antioxidant glutathione (GSH). GSH rescues cells from prooxidant-induced lung injury associated with Nrf2 deficiency. Results provide insight into the molecular mechanisms by which Nrf2 regulates cellular protection and proliferation.

Organism:: Mus musculus

Type:: Expression profiling by array, count, 2 agent, 2 genotype/variation sets

Platform:: GPL1261
Series:: GSE7810
6 Samples

Download data: CEL

DataSet

Accession:: GDS2875

ID:: 2875

Select item 20008735715.

Global mapping of binding sites for Nrf2 identifies novel targets in cell survival response through ChIP-Seq profiling and network analysis

(Submitter supplied) The Nrf2 (nuclear factor E2 p45-related factor 2) transcription factor responds to diverse oxidative and electrophilic environmental stresses by circumventing repression by Keap1, translocating to the nucleus, and activating cytoprotective genes. Nrf2 responses provide protection against chemical carcinogenesis, chronic inflammation, neurodegeneration, emphysema, asthma and sepsis in murine models. Nrf2 regulates the expression of a plethora of genes that detoxify oxidants and electrophiles and repair or remove damaged macromolecules, such as through proteasomal processing. However, many direct targets of Nrf2 remain undefined. Here, mouse embryonic fibroblasts (MEF) with either constitutive nuclear accumulation (Keap1−/−) or depletion (Nrf2−/−) of Nrf2 were utilized to perform chromatin-immunoprecipitation with parallel sequencing (ChIP-Seq) and global transcription profiling. This unique Nrf2 ChIP-Seq dataset is highly enriched for Nrf2-binding motifs. Integrating ChIP-Seq and microarray analyses, we identified 645 basal and 654 inducible direct targets of Nrf2, with 244 genes at the intersection. Modulated pathways in stress response and cell proliferation distinguish the inducible and basal programs. Results were confirmed in an in vivo stress model of cigarette smoke-exposed mice. This study reveals global circuitry of the Nrf2 stress response emphasizing Nrf2 as a central node in cell survival response.

Organism:: Mus musculus

Type:: Genome binding/occupancy profiling by high throughput sequencing

Platform:: GPL9185
3 Samples

Download data: TXT, WIG

Series

Accession:: GSE87357

ID:: 200087357

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20002963216.

Effect of Nrf2 deletion in postnatal lung development and BPD phenotype in newborn mice

(Submitter supplied) Background: Nrf2 is an essential cytoprotective transcription factor. However, association of Nrf2 in organ development and neonatal disease is rarely examined. Hyperoxia exposure to newborn rodents generates pulmonary phenotypes which resemble bronchopulmonary dysplasia (BPD) of prematurity. Methods: To investigate the role of Nrf2 in lung maturation and BPD pathogenesis, Nrf2-deficient (Nrf2-/-) and wild-type (Nrf2+/+) neonates were exposed to air or hyperoxia (O2). more...

Organism:: Mus musculus

Type:: Expression profiling by array

Platform:: GPL1261
42 Samples

Download data: CEL

Series

Accession:: GSE29632

ID:: 200029632

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Select item 20007551317.

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

PubMed Full text in PMC Similar studies SRA Run Selector

Select item 20019395818.

Comprisons of lung tissue gene expression from AKR and C57BL/6 mice exposed to Cigarette smoke and LPS in ARDS/ALI mice model

(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

Series

Accession:: GSE193958

ID:: 200193958

PubMed Full text in PMC Similar studies Analyze with GEO2R

Select item 20000920819.

Genetic and Pharmacologic Evidence Links Oxidative Stress to Ventilator-Induced Lung Injury in Mice

(Submitter supplied) RATIONALE: Mechanical ventilation (MV) is an indispensable therapy for critically ill patients with acute lung injury and the adult respiratory distress syndrome. However, the mechanisms by which conventional MV induces lung injury remain unclear. OBJECTIVES: We hypothesized that disruption of the gene encoding Nrf2, a transcription factor which regulates the induction of several antioxidant enzymes, enhances susceptibility to ventilator-induced lung injury (VILI), while antioxidant supplementation attenuates such effect. more...