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MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 5 days daily and 5 days daily exposure followed by 3 days washout.

ABSTRACT: MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 5 days daily and 5 days daily exposure followed by 3 days washout.

PROVIDER: PRJEB12749 | ENA |

REPOSITORIES: ENA

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			Action	DRS
		Other
	ERR1273740.fastq.gz	Fastqsanger.gz
	ERR1273750.fastq.gz	Fastqsanger.gz
	ERR1273741.fastq.gz	Fastqsanger.gz
	ERR1273751.fastq.gz	Fastqsanger.gz

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Protein data in PHH after VPA-treatment

Project description:LC-MS/MS protein data of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

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RNA-seq of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

Project description:Primary Human Hepatocytes (PHH) were exposed daily for 3 days to 15 mM VPA after which RNA was isolated. After terminating the VPA treatment, part of the cells were kept with medium for 3 days in order to investigate the eventual persistence of VPA-induced methylome changes. Identification of differentially expressed regions in the RNA was carried out by the RNA-seq method.

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Project description:RNA-seq of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

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MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 5 days daily and 5 days daily exposure followed by 3 days washout.

Project description:Primary Human Hepatocytes (PHH) were exposed daily for 5 days to 15 mM VPA after which DNA was isolated. After terminating the VPA treatment, part of the cells were kept with medium for 3 days in order to investigate the eventual persistence of VPA-induced methylome changes. Identification of methylated regions in the DNA was carried out by the Methylated DNA Immuno-Precipitation - sequencing (MeDIP-seq) method and contains the following steps: fragmentation, library preparation, MeDIP, and sequencing.

2017-09-25 | E-MTAB-4437 | biostudies-arrayexpress

MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

Project description:Primary Human Hepatocytes (PHH) were exposed daily for 3 days to 15 mM VPA after which DNA was isolated. After terminating the VPA treatment, part of the cells were kept with medium for 3 days in order to investigate the eventual persistence of VPA-induced methylome changes. Identification of methylated regions in the DNA was carried out by the Methylated DNA Immuno-Precipitation - sequencing (MeDIP-seq) method and contains the following steps: fragmentation, library preparation, MeDIP, and sequencing.

2018-02-23 | E-MTAB-5983 | biostudies-arrayexpress

MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

Project description:MeDIP profiling by high-throughput sequencing of Primary Human Hepatocytes (PHH) exposed to Valproic Acid (VPA) for 3 days daily and 3 days daily exposure followed by 3 days washout.

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Induction of miRNA changes in primary human hepatocytes by valproic acid

Project description:Valproic acid (VPA) is a very potent anti-cancer and neuro-protective drug. However, exposure to VPA may cause accumulation of lipids in the liver which could result in the development of steatosis. As VPA is a fatty acid analogue, most of the performed studies focus on inhibition of the mitochondrial b-oxidation pathway as the possible mode of action. However, investigations exploring the contribution of other processes in particular by using whole genome studies in a relevant human liver model are limited. Furthermore, the contribution of gene expression regulation by DNA methylation changes and/or miRNA changes is hardly known. Therefore, in the present study, we investigated the effect of repetitive VPA exposure on primary human hepatocytes (PHH) on whole genome gene expression-, DNA methylation-, and miRNA changes, using microarrays and integrated data analyses. PHH were exposed to a non-cytotoxic dose of 15 mM VPA for 5 days daily thereby inducing accumulation of lipids. Part of the PHH was left untreated for an additional 3 days in order to study the persistence of changes. VPA modulated the expression of a number of nuclear receptors and their target genes, leading to disturbed fatty acid metabolism and - uptake, ultimately leading to accumulation of triglycerides in the liver which is the key event leading to steatosis. Part of the gene expression changes was epigenetically regulated. Furthermore, after terminating the treatment, the expression and DNA methylation changes of several genes remained persistent, indicating a permanent change in the PHH, causing steatosis development to continue and/or making the PHH more sensitive for steatosis development during a subsequent exposure.

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Project description:Interindividual differences in hepatic metabolism, which are mainly due to genetic polymorphism in its gene, have a large influence on individual drug efficacy and adverse reaction. Hepatocyte-like cells (HLCs) differentiated from human induced pluripotent stem (iPS) cells have the potential to predict interindividual differences in drug metabolism capacity and drug response. However, it remains uncertain whether human iPSC-derived HLCs can reproduce the interindividual difference in hepatic metabolism and drug response. We found that cytochrome P450 (CYP) metabolism capacity and drug responsiveness of the primary human hepatocytes (PHH)-iPSHLCs were highly correlated with those of PHHs, suggesting that the PHH-iPS-HLCs retained donor-specific CYP metabolism capacity and drug responsiveness. We also demonstrated that the interindividual differences, which are due to the diversity of individual SNPs in the CYP gene, could also be reproduced in PHH-iPS-HLCs. We succeeded in establishing, to our knowledge, the first PHH-iPS-HLC panel that reflects the interindividual differences of hepatic drugmetabolizing capacity and drug responsiveness.

2014-11-12 | GSE61287 | GEO

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