Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Microcystin-LR prenatal exposure induces coronary heart disease through macrophage polarization imbalance mediated by trophoblast-derived extracellular vesicles.

ABSTRACT: Trophoblast-derived extracellular vesicles (T-EVs) increase during pregnancy and act as a critical signal in macrophage polarization. However, MC-LR significantly affected the miRNA expression profile of T-EVs. Upon internalization into macrophages, T-EVs-derived miR-377-3p specifically targets the 3’UTR region of NR6A1 to inhibit the gene expression. Silencing of transcription suppressor NR6A1 leads to abnormal activation of the downstream mTOR/S6K1/SREBP pathway, inducing metabolic reprogramming and ultimately leading to M1 polarization of macrophages.

ORGANISM(S): Homo sapiens

PROVIDER: GSE266672 | GEO | 2025/04/25

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Microarray Analysis of Microcystin-LR

Project description:Microcystins are produced by the cyanobacteria, most commonly Microcystis aerµginosa. Upon ingestion, toxic microcystins are actively absorbed by fish, birds and mammals where they are primarily liver toxins. Groups of 4-6 rats were exposed to 0, 1, 10, 50 or 100 µg/kg microcystin-LR for 0.5, 1, 3 or 6 hours and gene expression analysis performed on liver with samples hybridized to whole rat genome RG230_2.0 GeneChip arrays (Affymetrix, CA).

2014-07-25 | E-GEOD-59495 | biostudies-arrayexpress

Transcriptional and Behavioral Responses of Zebrafish Larvae to Microcystin-LR Exposure

Project description:Microcystin-LR (MC-LR), the most toxic member of microcystin family, inhibits protein phosphatase PP2A, triggers oxidative stress and induces hepatotoxicity. Gene expression profiling of MC-LR treated larvae using DNA microarray analysis revealed effects in the retinal visual cycle and pigmentation synthesis pathways that have not been previously associated with MC-LR. Liver-related genes were also differentially expressed. The microarray data were confirmed by quantitative real-time PCR. Our findings provide new evidence that microcystin-LR exposure of zebrafish larvae modulates the retinal visual cycle and pigmentation synthesis pathways and ultimately alter larval zebrafish behavior

2017-02-16 | GSE73739 | GEO

Differentially expressed genes in the livers of mice exposed to microcystin-LR (MC-LR)

Project description:To explore the molecular mechanisms involved in the toxicity in the livers exposed to MC-LR at the environmental level, the hepatic transcriptome was performed. A total of 210 genes were differentially expressed (P<0.05, |fold change|≥2) in response to MC-LR exposure; among them, 143 genes were significantly upregulated, and 67 genes were downregulated. Pathway enrichment analysis identified the top biological functions associated with the genes differentially expressed in response to MC-LR exposure, which were circadian regulation of gene expression, negative regulation of glucocorticoid receptor signaling pathway, the epoxygenase P450 pathway, regulation of insulin secretion, lipid metabolic process, and cell cycle pathway.

2020-03-25 | GSE145459 | GEO

Global transcriptomic profiling of microcystin-LR or -RR treated hepatocytes (HepaRG)

Project description:Microcystins (MC) are toxins found in harmful algal blooms. The canonical MC mode of action (MOA) is the inhibition of protein phosphatases, but complete characterization of its toxicity pathway has yet to be identified. The existence of 100s of MC structural congeners further complicates risk estimates. This work employed RNA-seq to provide an unbiased and comprehensive characterization of cellular targets and impacted cellular processes of hepatocytes exposed to either MC-LR or MC-RR congeners. The human hepatocyte cell line, HepaRG, was treated with three concentrations of MC-LR or RR (1000, 100, 10 g/L) for two hours. Significant reduction in cell survival was observed in the LR1000 and LR100 treatments. RNA-seq was performed on the control groups and all concentrations of MC-LR and -RR and differentially expressed genes (DEGs) were identified. Genes and pathways associated with oxidative and endoplasmic reticulum stress, and the unfolded protein response (UPR) were highly enriched by both congeners. Enrichment of inflammatory pathways was also evident. In the cytotoxic LR1000 treatment, apoptotic pathways and related genes were identified, suggesting cells pursue both inflammation and apoptosis simultaneously and that cellular fate may be determined by the activation kinetics of jun N-terminal kinase (JNK). We present a model of MC toxicity where MCs cause the production of ROS and oxidative stress leading to ER stress and activation of the UPR. Under non-cytotoxic conditions this leads to an inflammatory and pro-survival cellular response mediated through up-regulation and activation of NF- and its inhibition of JNK. With acute MC exposure, increased ER stress results in the cellular program switching to favor apoptosis by inhibiting NF- resulting in sustained JNK activation and through the activation of C/EBP homologous protein (CHOP) via the protein kinase RNA-like endoplasmic reticulum kinase (PERK) arm of the UPR

2021-03-09 | GSE147999 | GEO

Microcystin-LR prenatal exposure induces coronary heart disease through macrophage polarization imbalance mediated by trophoblast-derived extracellular vesicles.

Project description:Microcystin-LR prenatal exposure induces coronary heart disease through macrophage polarization imbalance mediated by trophoblast-derived extracellular vesicles.

| PRJNA1108245 | ENA

Alteration of MicroRNA Expression Profile Linked to Microcystin-LR-Induced Tumorigenicity in Human WRL-68 Cell Line

Project description:We report microcystin-LR, a cyclic heptapeptide that acts as a potent hepatotoxin and carcinogen, was used to induce the malignant transformation of the WRL-68 cell line and alterations in microRNA (miRNA) expression in the transformed cells. In this work, MC-LR was used to induce the malignant transformation of the WRL-68 cell line and alterations in microRNA (miRNA) expression in the transformed cells.

2012-07-30 | E-GEOD-30560 | biostudies-arrayexpress

Differentially expressed genes in the livers of mice exposed to microcystin-LR (MC-LR)

Project description:Differentially expressed genes in the livers of mice exposed to microcystin-LR (MC-LR)

| PRJNA607252 | ENA

Transcriptome analysis of Novosphingobium sp. THN1 during microcystin-LR degradation under different carbon concentrations

Project description:The bacterium Novosphingobium sp. THN1 (THN1) is capable of degrading microcystin-LR (MCLR). To get an insight into genes expression during MCLR degradation and the regulation of different carbon concentrations on MCLR degradation, we performed RNA-seq of THN1 during MCLR degradation under different carbon concentrations.

2019-01-30 | GSE125827 | GEO

Alteration of MicroRNA Expression Profile Linked to Microcystin-LR-Induced Tumorigenicity in Human WRL-68 Cell Line

2012-07-31 | GSE30560 | GEO

Effect of Microcystin-LR and cylindrospermopsin (CYN) on gene expression in human hepatocytes, HepaRG cells and HCC HepG2 cells.

Project description:Human hepatocytes, HepaRG cells and HCC HepG2 cells were treated with 50nM of Microcystin-LR and cylindrospermopsin (CYN) to observe changes in gene expression.

2023-05-12 | E-MTAB-12881 | biostudies-arrayexpress

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