Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [PRO-seq]

ABSTRACT: Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [PRO-seq]

PROVIDER: PRJNA704407 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR13772348.fastq.gz	Fastqsanger.gz
	SRR13772349.fastq.gz	Fastqsanger.gz
	SRR13772350.fastq.gz	Fastqsanger.gz
	SRR13772351.fastq.gz	Fastqsanger.gz
	SRR13772352.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 6

Similar Datasets

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles

Project description:Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles

| PRJNA704405 | ENA

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [PRO-seq]

Project description:Transcriptional responses to wildfire smoke, an increasingly important cause of human morbidity, are poorly understood. Here, using a combination of precision nuclear run-on sequencing (PRO-seq) and the assay for transposase-accessible chromatin using sequencing (ATAC-seq), we identify rapid and dynamic changes in transcription and chromatin structure in Beas-2B airway epithelial cells after exposure to wood smoke particles (WSP). By comparing 30 and 120 minutes of WSP exposure, we defined three distinct temporal patterns of transcriptional induction and chromatin responses to WSP. Whereas transcription of canonical targets of the aryl hydrocarbon receptor (AHR), such as CYP1A1 and AHRR, was robustly increased after 30 minutes of WSP exposure, transcription of these genes and associated enhancers returned to near baseline at 120 minutes. ChIP-qPCR assays and AHR knockdown confirmed a role for AHR in regulating these transcriptional responses, and we applied bioinformatics approaches to identify novel AHR-regulated pathways and targets including the DNA methyltransferase, DNMT3L, and its interacting factor, SPOCD1. Our analysis also defined a role for NFkB as a primary transcriptional effector of WSP-induced changes in gene expression. The kinetics of AHR- and NFkB-regulated responses to WSP were distinguishable based on the timing of both transcriptional responses and chromatin remodeling, with induction of several cytokines implicated in maintaining the NFkB response. In aggregate, our data establish a direct and primary role for AHR in mediating airway epithelial responses to WSP and identify crosstalk between AHR and NFkB signaling in controlling pro-inflammatory gene expression.

2021-02-24 | GSE167371 | GEO

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [ATAC-seq]

2021-02-24 | GSE167370 | GEO

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [ATAC-seq]

Project description:Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles [ATAC-seq]

| PRJNA704406 | ENA

Nascent RNA sequencing defines dynamic aryl hydrocarbon receptor signaling responses to wood smoke particles

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

2021-02-24 | GSE167372 | GEO

Effects of Smoldering Eucalyptus Wood Smoke Extract on Primary Human Brain Microvascular Endothelial Cells (HBMEC) and Immortalized Human Cerebral Microvascular Endothelial Cell Line (hCMEC/D3)

Project description:Increase in frequency and size of wildfire raises a significant public health concern due to rapid climate change. Epidemiological studies have shown that wildfire smoke exposure can increase the risk of neurological disorders. Our study aims to understand how wildfire smoke particles affect brain endothelial cells using both primary human brain microvascular endothelial cells (HBMEC) and an immortalized human cerebral microvascular endothelial cell line (hCMEC/D3). HBMEC and hCMEC/D3 were exposed to different levels of smoldering eucalyptus smoke particles (10, 30, 50 ug/mL) for 24 hr. Supernatants were collected for LDH and ELISA array, cell lysates were collected for RNAseq, and cells were fixed and stained for tight junction marker (Zonula Occludens-1, ZO-1) via ICC. Our study found that treatment to smoldering eucalyptus particles can increase inflammatory cytokine production dose-dependently in HBMECs and hCMEC/D3. Moreover, RNAseq analyses resulted in dose-dependent changes in HBMEC and hCMEC/D3 from wood smoke treatment that could be mediated via AhR and Nrf2 pathways.

2024-10-02 | GSE271935 | GEO

Examining the potential protective effect of Vasaka tea extract on lung cells exposted to Pine wood smoke

Project description:This study tested the hypothesis that a medicinal plant, Vasaka, typically consumed as a tea to treat respiratory malaise, could protect airway epithelial cells (AECs) from wood smoke particle-induced damage and prevent pathological mucus expression. Wood/biomass smoke is a common pneumotoxic air pollutant that activates transient receptor potential ankyrin 1 (TRPA1) and causes endoplasmic reticulum (ER) stress and AEC damage. This stimulates epidermal growth factor receptor and mucin 5AC (MUC5AC) production by AECs. Mucus normally protects the airways, but excessive MUC5AC production can obstruct airflow and cause respiratory distress. Vasaka tea pre- and co-treatment dose-dependently inhibited MUC5AC mRNA induction in cells treated with wood smoke particles. This correlated with TRPA1 inhibition, an attenuation of ER stress, and AEC damage/death, among other effects. Induction of mRNA for Anterior Gradient 2 (AGR2), an ER chaperone/disulfide isomerase required for MUC5AC production, and TRP vanilloid-3 (TRPV3), a gene that suppresses ER stress and wood smoke particle-induced cell death, were also attenuated. Variable inhibition of TRPA1, ER stress, and MUC5AC mRNA induction was observed using selected chemicals identified in Vasaka tea including vasicine, vasicinone, apigenin, 9-oxoODE, and 9,10-EpOME. 9,10-EpOME and apigenin were the most cytoprotective and mucosuppressive. Cytochrome P450 1A1 mRNA was also induced by Vasaka tea and wood smoke particles. Inhibition of CYP1A1 enhanced ER stress and MUC5AC mRNA expression, suggesting a role in producing protective oxylipins in stressed cells. The results provide mechanistic insights and support for the purported benefits of Vasaka tea in treating lung inflammatory conditions, raising the possibility of further development as a preventative therapy.

2023-07-05 | GSE232172 | GEO

The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries

Project description:This SuperSeries is composed of the following subset Series: GSE15857: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Kidney GSE15858: The Aryl Hydrocarbon Receptor Regulates Tissue-Specific Dioxin-Dependent and Dioxin-Independent Gene Batteries: Liver Refer to individual Series

2010-05-05 | E-GEOD-15859 | biostudies-arrayexpress

Activation of aryl hydrocarbon receptor

Project description:VAF347 is a low molecular weight compound which inhibits allergic lung inflammation in vivo. This effect is likely due to a block of dendritic cell (DC) function to generate pro-inflammatory T-helper (Th) cells since VAF347 inhibits IL-6, CD86 and HLA-DR expression by human monocyte derived DC, three relevant molecules for Th-cell generation. Here we demonstrate that VAF347 interacts with the aryl hydrocarbon receptor (AhR) protein resulting in activation of the AhR signaling pathway. Functional AhR is responsible for the biological activity of VAF347 since, i) other AhR agonists display an identical activity profile in vitro, ii) gene silencing of wild type AhR expression or forced over-expression of a trans-dominant negative AhR ablates VAF347 activity to inhibit cytokine induced IL-6 expression in a human monocytic cell line and iii) AhR deficient mice are resistant to the compound’s ability to block allergic lung inflammation in vivo. These data identify the AhR protein as key molecular target of VAF347 and its essential role for mediating the anti-inflammatory effects of the compound in vitro and in vivo. Keywords: effect of compound

2008-02-12 | GSE10463 | GEO

Chronic Aryl Hydrocarbon Receptor Activity Causes Adverse Muscle Affect: Implications for Smoking-induced Muscle Impairment

Project description:Purpose: The goal of this study was to analyze the gene expression levels by RNA sequencing from the plantaris muscle of mice exposed to normal air or tobacco smoke for 16 weeks. Methods: Plantaris muscles were removed, flash frozen, and RNA was harvested using the RNeasy Tissue Mini Kit (Qiagen), according to manufacturer’s instructions. RNA was reverse transcribed to complementary DNA (Lexogen QuantSeq 3′ FWD), and sequenced on a HiSeq 4000 instrument (Illumina). Results: Gene clusters representing neurogenesis/axon development, neuronal projection/synapse, and myofibril/sarcomere/muscle differentiation were amongst the most affected by chronic tobacco smoke exposure. In addition, mitochondrial network genes and neuromuscular genes were down-regulated in smoke-exposed mice. Conclusions: Chronic tobacco smoke exposure in mice reprograms the skeletal muscle transcriptome, with a reduction in mitochondrial and neuromuscular junction genes being consistent with mitochondrial respiratory impairment and neuromuscular junction degeneration observed at whole tissue level.

2020-10-23 | GSE151099 | 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