Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Human Preadipocyte Response to PCB126

ABSTRACT: Human Preadipocyte Response to PCB126

PROVIDER: PRJNA796625 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR17596400_1.fastq.gz	Fastqsanger.gz
	SRR17596400_2.fastq.gz	Fastqsanger.gz
	SRR17596401_1.fastq.gz	Fastqsanger.gz
	SRR17596401_2.fastq.gz	Fastqsanger.gz
	SRR17596402_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 46

Similar Datasets

Human Preadipocyte Response to PCB126

Project description:Purpose: The goal of this study was to perform an expression transcript profile over a timecourse of human preadipocytes that were treated with PCB126; Methods: Immortal human preadipocytes (NPAD) were treated with 10 uM PCB126 for 9 hrs, 1 day, or 3 days. RNA was extracted with TriZol, DNase treated, and purified using a Qiagen column. RNAseq was used to assess gene expression. Bioinformatic analyses were used to determine differential gene expression between PCB126 treated and vehicle-treated at the same timepoint.

2022-05-24 | GSE193578 | GEO

Human Preadipocyte Response to PCB52 or 4-OH-PCB52

Project description:Human Preadipocyte Response to PCB52 or 4-OH-PCB52

| PRJNA847891 | ENA

Transcription profiling of rat liver after 13 weeks of subchronic exposure to TCDD, PeCDF, PCB126, PCB153 and PCB126/PCB153

Project description:This study investigates the effects of the aryl hydrocarbon receptor (AhR) ligands TCDD, PCB126 and PeCDF; the non-AhR ligand PCB153 and the binary mixture PCB126/PCB153 on hepatic gene expression in female sprague dawley rats. Rats were treated with toxicological equivalent doses of TCDD (100ng/kg), PeCDF (200ng/kg), PCB126 (1000ng/kg) and PCB153 (1000ug/kg) 5 days a week for 13 weeks. Experiment Overall Design: There are 6 control chips and representing animals treated with vehicle control. There are 3 biological replicates (3 chips) for each treatment group (eg. TCDD, PCB126), each biological replicate is derived from 2 individual animals. A total of 21 chips were analyzed. Intensities were normalized using the GC-Robust Multiarray (GCRMA) method through Genetraffic software package.

2008-06-14 | E-GEOD-5789 | biostudies-arrayexpress

Imortalized mouse preadipocyte response to Il13 pre-treatment

Project description:Imortalized mouse preadipocyte response to Il13 pre-treatment

| PRJNA720306 | ENA

Effect of 13 weeks of subchronic exposure to TCDD, PeCDF, PCB126, PCB153 and PCB126/PCB153 on hepatic gene expression

2006-09-08 | GSE5789 | GEO

Single-cell transcriptomic analysis of mouse liver reveals nonparenchymal cells' intricate responses to PCB126 exposure

Project description:Polychlorinated biphenyls (PCBs) are ubiquitous and representative pollutants that pose great health risks. While cells' responses to dioxin-like PCBs tend to be studied on a bulk scale, few studies have been made from a single-cell level. Here, by using single-cell RNA sequencing, we depicted a detailed landscape of hepatic nonparenchymal cells' intricate responses to PCB126 exposure. A total of 13 clusters were identified. Notably, PCB126 exposure resulted in cell-type-specific gene expression profiles and genetic pathways. By analyzing genes related to aryl hydrocarbon receptors, we discovered that PCB126 induced the canonical genomic AhR pathway mainly in endothelial cells. In contrast, other cell types showed little induction. Enrichment pathway analysis indicated that immune cells changed their transcriptional patterns in response to PCB126. ScRNA-seq is a powerful tool to dissect underlying mechanisms of chemical toxicity regarding biological heterogeneity. Taken together, our study not only extends our current understanding of PCB126 toxicity, but also emphasizes the importance of in vivo cell heterogeneity in environmental toxicology.

2023-02-11 | GSE190084 | GEO

Primary human preadipocyte differentiation using bulk RNA-sequencing

Project description:Primary human preadipocyte differentiation using bulk RNA-sequencing

| PRJNA1047650 | ENA

Primary human preadipocyte differentiation using bulk RNA-sequencing

Project description:We performed bulk RNA-sequencing on primary human preadipocytes in which we induced differentiation, and collected samples at 6 timepoints across 14 days. The purpose of our study was to study gene expression during the course of preadipocyte differentiation into adipocytes.

2024-01-18 | GSE249195 | GEO

Identification of m6A-mediated changes in mouse liver after exposure to polychlorinated biphenyls (PCB126 and Aroclor1260) and high fat diet

Project description:Exposure to polychlorinated biphenyls (PCBs) has been associated with liver injury in human cohorts and with nonalcoholic steatohepatitis (NASH) in mice fed a high fat diet (HFD). N(6)-methyladenosine (m6A) modification of mRNA regulates transcript fate, but the contribution of m6A modification on regulation of transcription in PCB-induced steatosis and fibrosis is unknown. This study tested the hypothesis that PCB and HFD exposure alters the levels of m6A modification in transcripts that play a role in NASH in vivo. Male C57Bl6/J mice were fed a HFD (12 wks.) and administered a single oral dose of Aroclor1260, PCB126, or Aroclor1260 + PCB126. Genome-wide identification of m6A peaks was accomplished by m6A mRNA immunoprecipitation sequencing (m6A-RIP) and the mRNA transcriptome identified by RNA-seq. Exposure of HFD-fed mice to Aroclor1260 decreased the number of m6A peaks and m6A-containing genes relative to HFD control whereas PCB126 or the combination of Aroclor1260+PCB126 increased m6A modification frequency. ~ 41% of genes had one m6A peak and ~49% had 2-4 m6A peaks. 117 m6A peaks were common in the four experimental groups. The Aroclor1260 + PCB126 exposure group showed the highest number (52) of m6A-peaks. qRT-PCR confirmed enrichment of m6A-containing fragments of the Apob transcript with PCB exposure. Integrated analysis of m6A-RIP-seq and mRNA-seq identified 242 differentially expressed genes (DEGs) with increased or reduced number of m6A peaks. Comparative pathway analysis identified “Immune response: IL-6-induced acute-phase response in hepatocytes” in the Aroclor1260 + PCB126 samples, consistent with steatohepatitis in human PCB epidemiological studies. These data show that PCB exposure in HFD-fed mice alters the m6A landscape offering an additional layer of regulation of gene expression affecting a subset of gene responses in NASH.

2023-05-12 | GSE202386 | GEO

PCB126 Modifies the Murine Hepatic Transcriptome and Metallome to Promote Alcohol-associated Liver Disease Pathogenesis

Project description:Background: Environmental pollutants, including polychlorinated biphenyls (PCBs) have been shown to alter and promote the development of alcohol-associated liver disease (ALD). Our group recently demonstrated that PCB126 promoted steatosis, hepatomegaly, and modulated intermediary metabolism in an ALD rodent model. Objectives: To better understand how PCB126 promoted ALD, the current study adopts transcriptomic and metallomic approaches to identify mechanistic pathways involved in this promotion. Methods: Briefly, male C57BL/6J mice were exposed to 0.2 mg/kg PCB126 or corn oil vehicle prior to ethanol feeding in the chronic-binge model. Liver tissues were collected for RNA sequencing and ICP-MS metals quantification. Results: PCB126 uniquely modified the transcriptome in EtOH-fed mice in terms of variance. EtOH feeding alone resulting in >4000 differentially expressed genes (DEGs) and PCB126 exposure resulted in more DEGs in the EtOH-fed group over the pair-fed group. Top gene ontology (GO) biological processes indicated ‘peptidyl tyrosine modifications’ and GO molecular function processes showed a loss of ‘metal, and ion, and zinc binding’. Western blot analysis depicted that the JAK2-STAT5 signaling axis was disrupted by the enhanced loss of phosphorylated JAK2 in EtOH+PCB126 mice. Quantified liver essential metal levels were overall depleted by EtOH feeding, and potassium, magnesium, cobalt, and zinc were further decreased by PCB126. Discussion: The results suggests that phosphorylation and metal binding are disrupted in EtOH+PCB126 mice, implying that evolutionarily conserved homeostatic signaling mechanisms are modified by pollutant exposure in EtOH-fed mice. The loss of phosphorylation and essential metals are two suggestive modes of action that may explain the promotion of disease by PCB126 in ALD.

2024-05-01 | GSE244388 | 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