U.S. flag

An official website of the United States government

Format
Items per page
Sort by

Send to:

Choose Destination

Links from GEO DataSets

Items: 20

1.
Full record GDS5438

Lung from cigarette smoke-related chronic obstructive pulmonary disease model: time course

Analysis of lung from cigarette smoke (CS)-treated C57BL/6N females at 4 and 6 months of age. Tobacco smoking is a major cause of chronic obstructive pulmonary disease (COPD). Results provide insight into the molecular mechanisms underlying cigarette smoke-induced COPD.
Organism:
Mus musculus
Type:
Expression profiling by array, count, 2 age, 2 stress sets
Platform:
GPL6885
Series:
GSE52509
12 Samples
Download data
DataSet
Accession:
GDS5438
ID:
5438
2.

Cigarette smoke-induced iBALT mediates macrophage activation in a B cell-dependent manner in COPD

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is characterized by a progressive decline in lung function, caused by exposure to exogenous particles, mainly cigarette smoke (CS). COPD pathogenesis is initiated and perpetuated by an abnormal CS-induced inflammatory response of the lungs, involving both innate and adaptive immunity. Specifically, B cells organized in iBALT structures, as well as macrophages, accumulate in the lungs and contribute to CS-induced emphysema, but the mechanisms thereof remain unclear. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Dataset:
GDS5438
Platform:
GPL6885
12 Samples
Download data: TXT
Series
Accession:
GSE52509
ID:
200052509
3.

Expression data from the lungs of Scnn1b-Transgenic and wild-type mice

(Submitter supplied) Airway mucus obstruction triggers macrophage activation and MMP12-dependent emphysema
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6246
6 Samples
Download data: CEL
Series
Accession:
GSE49373
ID:
200049373
4.

The non-canonical Notch ligand DNER regulates IFNγ in macrophages during COPD progression

(Submitter supplied) Chronic Obstructive Pulmonary Diseases (COPD) is the third leading cause of death worldwide with no curative therapy available. A novel non-canonical Notch ligand, DNER, has been identified in a GWAS to correlate with disease severity, but its function and contribution to COPD is completely unknown. DNER localization and expression was determined in COPD patients and 6 month cigarette smoke (CS)-exposed mice. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL16570
18 Samples
Download data: CEL
Series
Accession:
GSE119257
ID:
200119257
5.

MMP28 is a key contributor to emphysema pathogenesis

(Submitter supplied) Chronic Obstructive Pulmonary Disease, which is comprised of chronic bronchitis and emphysema, is a leading cause of morbidity and mortality. Because tissue destruction is the prominent characteristic of emphysema, extracellular proteinases, particularly those with elastolytic ability, are often considered to be key drivers in this disease. Several human and mouse studies have implicated roles for matrix metalloproteinases (MMPs), particularly macrophage-derived proteinases, in COPD pathogenesis. more...
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL6885
16 Samples
Download data: TXT
Series
Accession:
GSE93898
ID:
200093898
6.

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
7.

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
8.

Arginine methyltransferase regulates monocyte extravasation and function

(Submitter supplied) Extravasation of monocytes into tissue and to the site of injury is a fundamental immunological process underlying a variety of innate inflammatory responses across multiple organ systems, which requires rapid responses via post translational modifications (PTM) of proteins. Specifically, methylation of protein by arginine methyltransferases (PRMTs) is an epigenetic PTM implicated in inflammatory responses. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
16 Samples
Download data: H5AD, MTX, TXT
Series
Accession:
GSE185006
ID:
200185006
9.

Analysis of lung transcriptomic changes following inhibition of LTβR-signalling in cigarette smoke exposed mice

(Submitter supplied) How LTβR-signalling drives chronic tissue damage particularly in the lung, which mechanisms regulate this process, and whether LTβR-blockade might be of therapeutic value has remained unclear. To study the mechanisms underlying LTβR-inhibition, a transcriptional analysis was performed on lung tissue from B6 mice exposed to cigarette smoke for 6 months and treated therapeutically with LTβR-Ig from 4 to 6 months compared to mice exposed to cigarette smoke for 6 months and treated with control Ig from 4 to 6 months and filtered air control. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL21103
13 Samples
Download data: MTX, TXT
Series
Accession:
GSE151674
ID:
200151674
10.

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
11.

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
12.

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
13.

microarray analysis of lung SPC/GFP+ EpCAM+ cells from different smoke exposure mice

(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
Series
Accession:
GSE162919
ID:
200162919
14.

Gene expression in COPD and non-diseased nasopharyngeal organoids following Pseudomonas aeruginosa infection

(Submitter supplied) Pseudomonas aeruginosa is a common bacteria leading to exacerbations of chronic obstructive pulmonary disease (COPD) patients while this bacteria can be easily eradicated by the immune systems of healthy individuals. Human airway organoids derived from healthy individuals and COPD patients were infected with pseudomonas aeruginosa. This project aims (1) to understand the differences in gene expressions in healthy and COPD airway organoids during stable condition, without infection and (2) to investigate differential pathogenic mechanism (i.e. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
12 Samples
Download data: TXT
Series
Accession:
GSE201465
ID:
200201465
15.

COPD and non-diseased nasopharyngeal and bronchial organoids characterization by single cell RNA-seq

(Submitter supplied) Clinical COPD, characterised by intermittent and infective exacerbations, lacks cellular model systems for the study of host-pathogen relationships. We establish nasopharyngeal and bronchial organoids from COPD patients and healthy individuals. In contrast to healthy organoids, COPD organoids demonstrate the hallmark goblet cell hyperplasia phenotype with reduced ciliary beat frequency, leading to impaired mucociliary clearance. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL16791
4 Samples
Download data: MTX, TSV
Series
Accession:
GSE186017
ID:
200186017
16.

Role of Gq/11 and G12/13 signalling in Type II alveolar epithelial cells

(Submitter supplied) We have used microarrays to identify individual genes and pathways regulated by Gq/11 or G12/13 signalling in type II alveolar epithelial cells isolated from the lungs of knockout mice.
Organism:
Mus musculus
Type:
Expression profiling by array
Platform:
GPL1261
12 Samples
Download data: CEL, CHP
Series
Accession:
GSE87842
ID:
200087842
17.

Eosinophils promote lung emphysema via CTSL

(Submitter supplied) Patients with chronic obstructive pulmonary disease (COPD) having higher blood eosinophil levels exhibit worse lung function and more severe emphysema, implying the potential role of eosinophils in emphysema development. However, the specific mechanism underlying eosinophil-mediated emphysema development is not fully elucidated. In this study, single-cell RNA sequencing was used to identify eosinophil subgroups in mouse models of asthma and emphysema and analyze their functions. more...
Organism:
Mus musculus
Type:
Expression profiling by high throughput sequencing
Platform:
GPL24247
13 Samples
Download data: MTX, TSV
Series
Accession:
GSE237749
ID:
200237749
18.

Mucosal immune alterations at the early onset of tissue destruction in Chronic Obstructive Pulmonary Disease

(Submitter supplied) In 11 control (non-used donors) and 11 COPD (end-stage) explant frozen lungs, 4 cylinders/cores were processed per lung for microCT and tissue transcriptomics. MicroCT was used to quantify tissue percentage and alveolar surface density to classify the COPD cores in mild, moderate and severe zones, as well as to quantify terminal bronchioles. Transcriptomics of each core assessed fold changes in innate and adaptive cells and pathway enrichment score between control and COPD cores. more...
Organism:
Homo sapiens
Type:
Expression profiling by high throughput sequencing
Platform:
GPL17303
82 Samples
Download data: TXT
Series
Accession:
GSE239897
ID:
200239897
19.

Diesel exhaust particle (DEP)-treated HBE cells

(Submitter supplied) We evaluated the profile of lncRNA and mRNA expression in control and 50μg/ml DEP treated HBE cells using the Arraystar Human LncRNA Array v3.0 array,7th generation. Our findings implicates that dysregulation of mitochondria invovled mRNAs may play important role in cytotoxicity of DEP.
Organism:
Homo sapiens
Type:
Non-coding RNA profiling by array; Expression profiling by array
Platform:
GPL16956
6 Samples
Download data: TXT
Series
Accession:
GSE82335
ID:
200082335
20.

Cigarette smoking alters mRNA expression in human alveolar macrophages

(Submitter supplied) Alveolar macrophages from never smokers and active smokers were isolated by bronchoalveolar lavage and gene expression was measured. Chronic cigarette smoke exposure, as occurs in smoker's lungs, leads to significant changes in gene expression. Of note, RNA was isolated immediately following bronchoscopy. Alveolar macrophage levels were >95%.
Organism:
Homo sapiens
Type:
Expression profiling by array
Platform:
GPL5175
8 Samples
Download data: CEL
Series
Accession:
GSE34517
ID:
200034517
Format
Items per page
Sort by

Send to:

Choose Destination

Supplemental Content

db=gds|term=|query=1|qty=3|blobid=MCID_6649ec01f63069282756b471|ismultiple=true|min_list=5|max_list=20|def_tree=20|def_list=|def_view=|url=/Taxonomy/backend/subset.cgi?|trace_url=/stat?
   Taxonomic Groups  [List]
Tree placeholder
    Top Organisms  [Tree]

Find related data

Recent activity

Your browsing activity is empty.

Activity recording is turned off.

Turn recording back on

See more...
Support Center