GEO DataSets

(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) 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) 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) 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) 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) 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) 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

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

(Submitter supplied) The study aimed to compare the gene expression profiles at a single cell level in lung tissues between patients with COPD and donor controls.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL21103

8 Samples

Download data: CSV, MTX

(Submitter supplied) Lung aging triggers the onset of various chronic lung diseases, with alveolar repair being a key focus for alleviating pulmonary conditions. The regeneration of epithelial structures, particularly the differentiation from type II alveolar epithelial (AT2) cells to type I alveolar epithelial (AT1) cells, serves as a prominent indicator of alveolar repair. Nonetheless, the precise role of aging in impeding alveolar regeneration and the underlying mechanism remain to be fully elucidated. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

6 Samples

Download data: TXT

(Submitter supplied) Chronic obstructive pulmonary disease (COPD) is a progressive disease that obstructs the airflow from the lungs, and tobacco smoking is the major cause of COPD. Here, we applied single-cell RNA sequencing to analyze COPD pathogenesis in COPD patients, non-COPD smokers and never-smokers and investigated the disease progression at single-cell resolution. By single-cell transcriptome analysis, COPD was characterized by shifts in the stromal, immune system and epithelial cell compositions. more...

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL20795

16 Samples

Download data: MTX, RDS, TSV, TXT, XLSX

(Submitter supplied) Single cell RNA-sequencing (scRNAseq) of lung immune cells from mice exposed to room air or cigarette smoke, infected with influenza A virus. Room air saline controls are also included. This analysis facilitates a comparison of cigarette smoke-associated changes to the pulmonary immune environment at the level of individual leukocytes and stromal cells.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

3 Samples

Download data: H5

(Submitter supplied) Our study discusses the importance of studying sex-specific differences in the response of the airway epithelium to chronic injury. It focuses on tracheal epithelial cells from male and female mice exposed to chronic cigarette smoke and found evidence of sex-specific differences in gene expression and epithelial plasticity. Understanding these differences could lead to more effective personalized treatments for respiratory diseases.

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

24 Samples

Download data: CSV, GTF

(Submitter supplied) Alveolar epithelial cell fate decisions drive lung development and regeneration. Using transcriptomic and epigenetic profiling coupled with genetic mouse and organoid models, we identified Klf5 as a critical regulator of alveolar epithelial cell fate across the lifespan. During prenatal lung development and alveologenesis, Klf5 enforces alveolar epithelial type 1 (AT1) cell lineage fidelity. While it is dispensable for both adult AT1 and alveolar epithelial type 2 (AT2) cell homeostasis, Klf5 regulates AT2 cell plasticity after injury. more...

Organism:

Mus musculus

Type:

Expression profiling by high throughput sequencing

Platform:

GPL24247

9 Samples

Download data: CSV

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL21810

16 Samples

Download data: GPR

(Submitter supplied) We observed that loss of miR142 leads to the increased expression of surfactant protein C and decreased Podoplanin. This indicates increased differentiation of alveolar progenitors towards AEC II lineage. In order to understand what are the genes that are being regulated during AEC II cell differentiation in miR142 overexpressing mice we are performing this experiment.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL21810

8 Samples

Download data: GPR

(Submitter supplied) We observed that loss of miR142 leads to the increased expression of surfactant protein C and decreased Podoplanin.This indicates increased differentiation of alveolar progenitors towards AEC II lineage. In order to understand 1)what are the genes that are being regulated during AEC II cell differentiation in miR142KO mice we are performing this experiment.

Organism:

Mus musculus

Type:

Expression profiling by array

Platform:

GPL21810

8 Samples

Download data: GPR

(Submitter supplied) This SuperSeries is composed of the SubSeries listed below.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL30173

24 Samples

Download data

(Submitter supplied) We established a dual reporter (SFTPC:GFP AGER:mCherry-HiBiT) human iPSC line and the "On-Gel" spheroid culture system suitable for finding the essential signals for alveolar type 2 (AT2) to type 1 (AT1) cell conversion comprehensively. After compound screening, we found that LATS-IN-1 and BAY1125976 synergistically promoted AT1 marker gene expression.

Organism:

Homo sapiens

Type:

Expression profiling by high throughput sequencing

Platform:

GPL30173

12 Samples

Download data: CSV