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Global gene expression profiles in primary human hepatocytes exposed to phytochemicals

ABSTRACT: Primary human hepatocytes were treated with 2 non-cytotoxic concentrations of sulforaphane (SFN; 10 and 50 uM) phenethyl isothiocyante (PEITC; 10 and 25 uM), 3,3'-diindolylmethane (DIM; 10 and 50 uM), or one concentration of oltipraz (OPZ; 30 uM) for 48 hours. Given the considerable heterogeneity of the human population, it was essential that each experiment was performed with hepatocytes from the same liver, i.e. each liver served as its own control. Each treatment was performed on three batches of human hepatocytes, each derived from a separate liver. 32 arrays, 8 experimental groups.

ORGANISM(S): Homo sapiens

SUBMITTER: Richard Beyer

PROVIDER: E-GEOD-20479 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

Sulforaphane- and phenethyl isothiocyanate-induced inhibition of aflatoxin B1-mediated genotoxicity in human hepatocytes: role of GSTM1 genotype and CYP3A4 gene expression.

Gross-Steinmeyer Kerstin K Stapleton Patricia L PL Tracy Julia H JH Bammler Theo K TK Strom Stephen C SC Eaton David L DL

Toxicological sciences : an official journal of the Society of Toxicology 20100504 2

Primary cultures of human hepatocytes were used to investigate whether the dietary isothiocyanates, sulforaphane (SFN), and phenethyl isothiocyanate (PEITC) can reduce DNA adduct formation of the hepatocarcinogen aflatoxin B(1) (AFB). Following 48 h of pretreatment, 10 and 50 microM SFN greatly decreased AFB-DNA adduct levels, whereas 25muM PEITC decreased AFB-DNA adducts in some but not all hepatocyte preparations. Microarray and quantitative reverse transcriptase (RT)-PCR analyses of gene expr ...[more]

PMID: 20442190

Similar Datasets

global gene expression profiles in primary human hepatocytes exposed to phytochemicals

Project description:Primary human hepatocytes were treated with 2 non-cytotoxic concentrations of sulforaphane (SFN; 10 and 50 uM) phenethyl isothiocyante (PEITC; 10 and 25 uM), 3,3'-diindolylmethane (DIM; 10 and 50 uM), or one concentration of oltipraz (OPZ; 30 uM) for 48 hours. Given the considerable heterogeneity of the human population, it was essential that each experiment was performed with hepatocytes from the same liver, i.e. each liver served as its own control. Each treatment was performed on three batches of human hepatocytes, each derived from a separate liver.

2010-07-19 | GSE20479 | GEO

Primary human hepatocytes treated with IFNalpha and IL28B

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with IFN, IL28b and T-PolyC after 6 or 24 hours respectively

2012-03-09 | E-GEOD-31264 | biostudies-arrayexpress

Primary human hepatocytes treated with IL28B and the HCV JFH1 Genotype 2A clone.

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with JFHA, and IL28b respectively with three biological replication.

2013-08-16 | E-GEOD-31455 | biostudies-arrayexpress

Transcription profiling by array of primary human hepatocytes derived from hepatitis C patients treated with type III interferons (IFNs) for 6 or 24 hours

Project description:Recent identification of IL28B gene polymorphisms associated with hepatitis C virus (HCV) clearance suggests a role for type III interferons (IFNs) in hepatitis C infection. The function of type III IFNs in intrinsic antiviral immunity is poorly understood. Here we show that HCV infection of primary human hepatocytes results in a robust induction of type III but not type I IFNs, leading to IFN- stimulated gene (ISG) expression. In addition, HCV infection elicits a much broader range of gene expression alterations in addition to ISG induction. The induction of type III IFNs is mediated by IRF3 and NFkB- dependent pathways. Type III IFN, aside from upregulating ISGs with a different kinetic profile, induces a distinct set of genes from type I IFN, potentially explaining the functional difference between the two types of IFNs. Chimpanzees undergoing experimental HCV infection demonstrated a prompt hepatic induction of IL28, associating with ISG upregulation, but minimal type I IFN induction. Analysis of liver biopsies from HCV-infected patients supported a close correlation among hepatic expression of IL28 and ISGs, but not with type I IFNs. Our study demonstrates that HCV infection results predominantly in type III IFN induction in the liver and the level of induction correlates with hepatic ISG levels, thus providing a mechanistic explanation for the association between IL28, ISG levels and recovery from HCV infection as well as a potential therapeutic strategy for the treatment of non-responders. Samples were treated with IFN or IL28b after 6 or 24 hours with three replications

2012-03-09 | E-GEOD-31193 | biostudies-arrayexpress

Effect of Chlorpromazine HCl on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with chlorpromazine HCl treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses (0.8 uM and 20 uM) of chlorpromazine HCl and 1% DMSO vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis. This series is part of a SuperSeries in which primary rat hepatocytes were treated with two doses of ten chemical compounds (and corresponding vehicle controls) for 24 and 48 hours. Each compound/vehicle treatment group was an individual study performed at different times. Each study was analyzed separately and themes common between studies were reported. Time Course/Dose Response

2012-08-28 | E-GEOD-40341 | biostudies-arrayexpress

Effect of Methapyrilene on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with methapyrilene treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses (3 uM and 100 uM) of methaphyriline and 1% DMSO vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis. This series is part of a SuperSeries in which primary rat hepatocytes were treated with two doses of ten chemical compounds (and corresponding vehicle controls) for 24 and 48 hours. Each compound/vehicle treatment group was an individual study performed at different times. Each study was analyzed separately and themes common between studies were reported. Time Course/Dose Response

2012-08-28 | E-GEOD-40347 | biostudies-arrayexpress

Effect of WY-14643 on Rat Primary Hepatocytes.

Project description:This study provides an evaluation of changes in gene expression associated with WY-14643 treatment of rat hepatocytes in vitro. Primary rat hepatocytes were treated for 24 and 48 hours with two doses 8 uM and 200 uM) of WY-14643 and 1% DMSO vehicle control. Five replicates of each treatment were performed. Cells were then extracted and RNA processed for microarray analysis. This series is part of a SuperSeries in which primary rat hepatocytes were treated with two doses of ten chemical compounds (and corresponding vehicle controls) for 24 and 48 hours. Each compound/vehicle treatment group was an individual study performed at different times. Each study was analyzed separately and themes common between studies were reported. Time Course/Dose Response

2012-08-28 | E-GEOD-40346 | biostudies-arrayexpress

Hepatocytes induces properties of wound healing type and regulatory macrophages in co-cultivated BMDM

Project description:The liver comprises the body´s largest pool of macrophages constituting approximately 80 % of all sessile tissue macrophages of the body. After liver damage monocyte-derived macrophages are recruited into the liver and were here affected by a micro milieu which is considerably influenced by hepatocytes. Up to now the complex network that determines the differentiation and function of liver macrophages and the impact of the intercellular communication between macrophages and the other parenchymal and non-parenchymal cell types of the liver is not well understood. The present study investigates the role of the intercellular communication between macrophages and hepatocytes on macrophage differentiation and function. Under physiological conditions the sinusoidal endothelial cell layer and the space of Dissé separate macrophages and hepatocytes from each other. Therefore the study focuses on the impact of the intercellular communication via soluble mediators on the differentiation of bone marrow derived macrophages (BMDM), which were recruited to the liver after liver injury, in co-culture models with highly purified primary murine hepatocytes embedded in a sandwich collagen matrix.

2023-07-07 | PXD012136 | Pride

Human Hepatocyte Proteome - In-depth quantitative analysis and comparison of the human hepatocyte and hepatoma cell line HepG2 proteomes

Project description:Here we report a comprehensive proteomic analysis of purified human hepatocytes and a human hepatoma cell line HepG2. The complete dataset comprises 9,400 proteins and provides quantitative depiction of the proteomes of hepatocytes and HepG2 cells at the protein titer and copy number dimensions.

2016-01-26 | PXD001874 | Pride

SIK2 phosphorylation in response to glucagon or insulin in murine hepatocytes

Project description:The phosphorylation state of human HA-tagged-SIK2, adenovirally introduced in murine hepatocytes (C57/BL/6 strain) was analysed in unstimulated and in response to glucagon- or insulin- treated conditions. Background:- LKB1 is a master kinase that regulates metabolism and growth through AMPK and 12 other closely-related kinases. Liver-specific ablation of LKB1 causes increased glucose production in hepatocytes in vitro and hyperglycaemia in fasting mice in vivo. The salt-inducible kinases (SIK1, 2 and 3), members of the AMPK-related kinase family, play a key role as gluconeogenic suppressor downstream of LKB1 in the liver. A selective SIK inhibitor (HG-9-91-01) promotes dephosphorylation of transcriptional co-activators CRTC2/3 resulting in enhanced gluconeogenic gene expression and glucose production in hepatocytes, an effect that is abolished when an HG-9-91-01-insensitive-mutant-SIK is introduced or LKB1 is ablated. Although SIK2 was proposed as a key regulator of insulin-mediated suppression of gluconeogenesis, we provide genetic evidence that liver-specific ablation of SIK2 alone has no effect on gluconeogenesis and insulin does not modulate SIK2 phosphorylation/activity. Collectively, we demonstrate that the LKB1-SIK pathway functions as a key gluconeogenic gatekeeper in the liver.

2014-08-08 | PXD001032 | Pride

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