Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Mus musculus

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

PROVIDER: PRJNA304448 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR2966800.fastq.gz	Fastqsanger.gz
	SRR2966810.fastq.gz	Fastqsanger.gz
	SRR2966820.fastq.gz	Fastqsanger.gz
	SRR2966801.fastq.gz	Fastqsanger.gz
	SRR2966811.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 31

Similar Datasets

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

Project description:Analysis of alveolar macrophage gene expression in C57BL6 wild-type and RAGE null mice exposed to cigarette smoke

2018-12-31 | GSE75513 | GEO

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

2016-02-16 | GSE77942 | GEO

Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

Project description:Human alveolar epithelial cells were exposed to cigarette smoke extract (CSE) for 1, 3 and 5 weeks at 1%, 5% and 10%, and gene expression was evaluated by complete transcriptome microarrays. In this study we explored the effect of cigarette smoke on the gene expression profile. Human alveolar epithelial cells stimulated with three different concentractions of CSE (1%, 5% and 10%) and for 1, 3 and 5 weeks were used for RNA extraction and hybridization on Affymetrix microarrays.

2016-02-16 | E-GEOD-77942 | biostudies-arrayexpress

Tobacco smoke exposure exacerbates silica-induced pulmonary toxicity in rats

Project description: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. Pulmonary toxicity and lung gene expression profiles were determined in male Fischer 344 rats exposed to air, crystalline silica, cigarette smoke or cigarette smoke plus crystalline silica. Silica exposure resulted in significant pulmonary toxicity which was further exacerbated by cigarette smoke exposure in the rats. Significant differences in the gene expression profiles were detected in the lungs of the rats exposed to cigarette smoke, silica or a combination of both compared with the control rats.

2020-11-01 | GSE136945 | GEO

Bulk RNA-seq of CRISPRi ADGRG6-kd iAT2 following cigarette smoke exposure

Project description:We performed bulk transcriptomic profiling of induced human pluripotent stem cells (iPSCs)-derived type 2 alveolar epithelial cells (iAT2). iPSCs stably expressed CRISPRi (dCas9-KRAB) under the control of doxycyline. iAT2s were transduced with a lentivirus expressing gRNA targeting the transcriptional start site of ADGRG6. Cells were treated with or without doxycyline to intiate CRISPRi-knockdown. Cells were plated at an air-liquid interface, then subsequently exposed to air or 5% cigarette smoke using a VitroCell smoke robot. Cells were harvested for bulk RNA sequencing 8 hours post cigarette smoke exposure

2023-09-20 | GSE223077 | GEO

Impact of curcumin on human monocytes (U937 cells) exposed to oxidative stress

Project description:Oxidative stress as a result of cigarette smoking is an important etiological factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic steroid-insensitive inflammatory disease of the airways. The activity of the transcriptional co-repressor Histone deacetylase-2 (HDAC2) is dramatically reduced in COPD and cells exposed to oxidative stress or cigarette smoke. Moreover, curcumin (diferuloylmethane), a dietary polyphenol, at concentrations upto 1uM specifically restores cigarette smoke extract (CSE)- or oxidative stress- impaired HDAC2 activity. The aim of this study was to therefore identify any links through those gene sets that are affected by oxidative stress and subsequent treatment with curcumin in order to determine whether or not this could explain the impact of curcumin on restoration of oxidant impaired HDAC2 transcriptional co-repressor activity. Keywords: time course

2008-03-20 | GSE10896 | GEO

Transcription profiling of human monocytes (U937 cell line) to assess the impact of curcumin on monocytes exposed to oxidative stress

Project description:Oxidative stress as a result of cigarette smoking is an important etiological factor in the pathogenesis of chronic obstructive pulmonary disease (COPD), a chronic steroid-insensitive inflammatory disease of the airways. The activity of the transcriptional co-repressor Histone deacetylase-2 (HDAC2) is dramatically reduced in COPD and cells exposed to oxidative stress or cigarette smoke. Moreover, curcumin (diferuloylmethane), a dietary polyphenol, at concentrations up to 1uM specifically restores cigarette smoke extract (CSE)- or oxidative stress- impaired HDAC2 activity. The aim of this study was to therefore identify any links through those gene sets that are affected by oxidative stress and subsequent treatment with curcumin in order to determine whether or not this could explain the impact of curcumin on restoration of oxidant impaired HDAC2 transcriptional co-repressor activity. Experiment Overall Design: Human PMA-differentiated U937 cells, unexposed or exposed to oxidative stress (100mM H2O2) were either left untreated or treated with curcumin (1 mM) for either 4 or 18 hr. Performed in triplicate

2009-12-17 | E-GEOD-10896 | biostudies-arrayexpress

Homo sapiens

Project description:Human alveolar epithelial cells (A549) exposed to cigarette smoke extract

| PRJNA312174 | ENA

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

Project description: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. In addition, we exposed wild type and miR-155 deficient mice to CS and show an attenuated inflammatory profile in the latter. Alveolar macrophages were sorted by FACS from the different experimental groups and their gene expression profile was analyzed by RNA sequencing. This analysis revealed increased expression of miR-155 targets (including the NF-κB inhibitor rassf6) and an attenuation of the CS-induced increase in inflammation-related genes in miR-155 deficient mice. Finally, intranasal instillation of a specific miR-155 inhibitor significantly attenuated the CS-induced pulmonary inflammation in mice. In conclusion, we highlight a role for miR-155 in CS-induced inflammation and the pathogenesis of COPD, implicating miR-155 as a new therapeutic target in COPD.

2019-12-16 | GSE137653 | GEO

Early-life exposure to tobacco smoke alters airway signaling pathways in D. melanogaster and later mortality in D. melanogaster

Project description:To investigate the effect of cigarette smoke exposure on gene expression in airway epithelial cells of Canton S Drosophila melanogaster larvae, we isolated the airways of cigarette smoke exposed larvae and air controls. We then performed gene expression profiling analysis using data obtained from RNA-seq of smoke-exposed males, smoke-exposed females, air-control males and air-control females. For each group 4 biological replicates were prepared, representing 40-50 larval airways.

2022-09-30 | GSE205093 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data