Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking

ABSTRACT: Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking

PROVIDER: PRJNA553135 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR9035410_1.fastq.gz	Fastqsanger.gz
	SRR9035410_2.fastq.gz	Fastqsanger.gz
	SRR9035420_1.fastq.gz	Fastqsanger.gz
	SRR9035420_2.fastq.gz	Fastqsanger.gz
	SRR9035411_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 88

Similar Datasets

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [array]

Project description:Background: The small airway epithelium (SAE, >6th generations), the initiation site of smoking-induced airway disorders, is highly sensitive to the stress of smoking. Due to variations over time in smoking habits, the SAE transcriptome fluctuates not only among smokers, but within each smoker. Averaging the HG-U133 Plus 2.0 transcriptome sampled 4 times in the same individuals over 1 yr enabled the identification of “public” smoking-dysregulated genes, i.e., genes consistently dysregulated within each smoker and shared by most smokers. Using an independent cohort of smokers assessed before and after quitting smoking, it was possible to assess the effect of smoking cessation on the “public” genes over time and identify a subset of genes that remain persistently abnormally expressed despite 12 months of smoking cessation.

2025-06-05 | GSE133923 | GEO

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [RNA-Seq]

2025-06-05 | GSE130967 | GEO

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [array]

Project description:Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [array]

| PRJNA553137 | ENA

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking

Project description:This SuperSeries is composed of the SubSeries listed below.

2025-06-05 | GSE133924 | GEO

Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [RNA-Seq]

Project description:Serial Sampling of the Small Airway Epithelium Over 1 Year in the Same Individuals to Identify “Public” Genes Commonly Dysregulated by Smoking [RNA-Seq]

| PRJNA542140 | ENA

Genetic Architecture of Smoking and Smoking Cessation

Project description:Genetic Architecture of Smoking and Smoking Cessation

| PRJNA75689 | ENA

16S rRNA sequencing of fecal samples from Atg16l1 T300A and wildtype littermate mice that were exposed to mainstream cigarette smoking co-housed with mice from the same genotype but not exposed to cigarette smoking

Project description:We found that mainstream cigarette smoking (4 cigarettes/day, 5 days/week for 2 weeks using Kentucky Research Cigarettes 3R4F) resulted in >20% decrease in the percentage of normal Paneth cell population in Atg16l1 T300A mice but showed minimal effect in wildtype littermate control mice, indicating that Atg16l1 T300A polymorphism confers sensitivity to cigarette smoking-induced Paneth cell damage. We performed cohousing experiments to test if Paneth cell phenotype is horizontally transmissible as is microbiota. Atg16l1 T300A and littermate controls that were exposed to cigarette smoking were used as microbiota donors, and these donor mice were exposed to smoking for 2 weeks prior to cohousing. Separate groups of Atg16l1 T300A and littermate controls that were not exposed to cigarette smoking were used as microbiota recipients. The microbiota recipients were co-housed with microbiota donors of the same genotype for 4 weeks, during this period the donors continued to be exposed to cigarette smoking. Cigarette smoking was performed using smoking chamber with the dosage and schedule as described above. At the end of the experiment, the fecal microbiota composition was analyzed by 16S rRNA sequencing.

2018-10-31 | E-MTAB-5720 | biostudies-arrayexpress

Burkholderia pseudomallei serial patient

Project description:Burkholderia pseudomallei serial patient

| PRJEB2119 | ENA

Persistence of Smoking-induced Dysregulation of Small Airway Epithelium miRNA Expression Despite Smoking Cessation

Project description:Rationale: Even after quitting smoking, the risk of the development of chronic obstructive pulmonary disease (COPD) and lung cancer remains significantly higher compared to never-smokers. Objectives: Based on the knowledge that COPD and most lung cancers start in the small airway epithelium (SAE), we hypothesized that smoking modulates miRNA expression in the SAE linked to the pathogenesis of smoking-induced airway disease, and that some of these changes persist after smoking cessation. Methods: SAE was collected from 10th to 12th order bronchi using fiberoptic bronchoscopy. Affymetrix miRNA 2.0 arrays were used to assess miRNA expression in the SAE from 10 healthy never-smokers and 10 healthy smokers, before and after they quit for 3 months. Smoking status was determined by urine nicotine and cotinine measurement. Results: There were significant differences in the expression of 34 miRNAs between healthy smokers and healthy never-smokers (p<0.01, fold-change >1.5), with functions associated with lung development, airway epithelium differentiation, inflammation and cancer. After quitting smoking for 3 months, 12 out of the 34 miRNAs did not return to normal levels, with Wnt/β-catenin signaling pathway the top enriched pathway of the target genes of the persistent deregulated miRNAs. Conclusions: In the context that many of these persistent smoking-dependent miRNAs are associated with differentiation, inflammation diseases or lung cancer, it is likely that persistent smoking-related changes in small airway epithelium miRNAs play a role in the subsequent development of these disorders.

2015-11-23 | GSE53519 | GEO

Gene Expression Circulating B Lymphocytes for Smoking Females

Project description:B cells were found to be directly associated with the onset and development of many smoking-induced diseases. However, the in vivo molecular response of B cells underlying the female cigarette smoking remains unknown. Using the genome-wide Affymetrix HG-133A GeneChip® microarray, we compared the gene expression profiles of peripheral circulating B cells between 39 smoking and 40 non-smoking healthy US white females.

2009-12-25 | GSE18723 | 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