Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Dissecting the cellular specificity of smoking effects and reconstructing lineages in the human airway epithelium

ABSTRACT: Dissecting the cellular specificity of smoking effects and reconstructing lineages in the human airway epithelium

PROVIDER: PRJNA554141 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR10668800_1.fastq.gz	Fastqsanger.gz
	SRR10668800_2.fastq.gz	Fastqsanger.gz
	SRR10668900_1.fastq.gz	Fastqsanger.gz
	SRR10668900_2.fastq.gz	Fastqsanger.gz
	SRR10668801_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 298

Similar Datasets

Dissecting the cellular specificity of smoking effects and reconstructing lineages in the human airway epithelium

Project description:Cigarette smoke first interacts with the lung through the cellularly diverse airway epithelium and goes on to drive development of most chronic lung diseases. Here, through single cell RNA-sequencing analysis of the tracheal epithelium from smokers and nonsmokers, we generate a comprehensive atlas of epithelial cell types and states, connect these into lineages, and define cell-specific responses to smoking. Our analysis infers multi-state lineages that develop into surface mucus secretory and ciliated cells and then contrasts these to the unique specification of submucosal gland (SMG) cells. Accompanying knockout studies reveal that tuft-like cells are the likely progenitor of both pulmonary neuroendocrine cells and CFTR-rich ionocytes. Our smoking analysis finds that all cell types, including protected stem and SMG populations, are affected by smoking through both pan-epithelial smoking response networks and hundreds of cell-specific response genes, redefining the penetrance and cellular specificity of smoking effects on the human airway epithelium.

2020-04-06 | GSE134174 | GEO

Dissecting the cellular specificity of smoking effects and reconstructing lineages in the human airway epithelium.

Project description: Not available

| S-EPMC7237663 | biostudies-literature

Genetic Architecture of Smoking and Smoking Cessation

Project description:Genetic Architecture of Smoking and Smoking Cessation

| PRJNA75689 | ENA

Reconstructing Prehistoric African Population Structure

Project description:Reconstructing Prehistoric African Population Structure

| PRJEB21878 | ENA

Transcriptional Response to WNT-inhibition-induced human cardiomyogenesis (single-cell RNA-seq)

Project description:Since embryonic cardiac development in vivo and in vitro cardiomyocyte differentiation protocols both require WNT inhibition, our study focussed on how inhibition of WNT signalling guides the transcriptional landscape towards human cardiomyocyte differentiation. We uncovered transcriptional responses using single-cell RNA sequencing. with bioinformatics analysis defining cell identities, reconstructing differentiation trajectories, dissecting WNT inhibition-dependent gene expression and inferring Gene Regulatory Networks (GRN) driving cardiomyocyte specification. We found that WNT inhibition (WNTi) redirects early mesoderm precursors towards a cardiomyocyte fate while limiting alternative lineages.

2026-06-08 | GSE333970 | GEO

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

Reconstructing gene regulatory networks of tumorigenesis

Project description:Reconstructing gene regulatory networks of tumorigenesis

| PRJNA294764 | ENA

Mycobacterium tuberculosis strain:Mtb lineages | isolate:Mtb lineages and sub-lineages

Project description:Mycobacterium tuberculosis strain:Mtb lineages | isolate:Mtb lineages and sub-lineages Genome sequencing and assembly

| PRJNA975069 | ENA

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

Tobacco smoking transcriptional imprinting contributes to urothelial cancer

Project description:Smoking is a major risk factor for Urothelial carcinoma (UC). However the complex mechanisms, how smoking promotes carcinogenesis and tumour progression, remain obscure. A microarray based approached was therefore performed to detect the smoking derived gene expression alteration in non-malignant and malignant urothelial tissues from patients with superficial or invasive UC. Smoking enhanced cell migration and response to tissue damages. In non-malignant tissues smoking induced immune response and altered the cytoskeleton. In urothelial carcinoma, smoking altered extracellular and chromosome structures. Smoking affected tissues from patients with invasive carcinomamore strongly, up-regulating particularly growth factors and oncogenes in non-malignant tissue of patients with invasive but not with superficial carcinoma. In former smokers, comparable changes were seen in tissues form patients with invasive disease while they were minor or reversed in tissue of patients with superficial disease. Best but not complete tissue repair was suggestedfor non-malignant tissue from patients with superficial tumours. we used microarray techniques to define gene expression profile which may explain the contribution of smoking to urothelial carcinoma.

2013-03-20 | GSE21142 | 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