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

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

PROVIDER: PRJEB61791 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	ERR11279136.fastq.gz	Fastqsanger.gz
	ERR11279137.fastq.gz	Fastqsanger.gz
	ERR11279138.fastq.gz	Fastqsanger.gz
	ERR11279139.fastq.gz	Fastqsanger.gz
	ERR11279140.fastq.gz	Fastqsanger.gz

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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.

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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

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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

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