Gene expression analysis of cardiomyocytes treated with a clinically relevant concentration of DEHP (50 ug/mL)
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ABSTRACT:
ORGANISM(S): Rattus norvegicus
SUBMITTER: Nikki Posnack
PROVIDER: E-GEOD-21640 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:We used microarrays to expression profile cardiomyocytes from neonatal Sprague-Dawley rats treated with 1 to 50 ug/mL DEHP and control (0.1% DMSO) to identify changes in gene expression related to connexin-43 expression, calcium handling, arrhythmogenesis and mechanical motion. Rat neonatal cardiomyocytes were treated with 1 ug/ml, 10 ug/ml, or 50 ug/ml DEHP (diluted in 0.1% DMSO) for 3 days, control samples were treated with 0.1% DMSO. Cardiomyocytes used in the experiments were from the same litter. Samples within a treatment group (control, DEHP) are biological replicates.
2010-09-01 | E-GEOD-21641 | biostudies-arrayexpress
Project description:We used microarrays to expression profile cardiomyocytes from neonatal Sprague-Dawley rats treated with 1 to 50 ug/mL DEHP and control (0.1% DMSO) to identify changes in gene expression related to connexin-43 expression, calcium handling, arrhythmogenesis and mechanical motion.
2010-09-01 | GSE21641 | GEO
Project description:We used microarrays to expression profile cardiomyocytes from neonatal Sprague-Dawley rats treated with 50 ug/mL DEHP and control (0.1% DMSO) to identify changes in gene expression related to connexin-43 expression, calcium handling, arrhythmogenesis and mechanical motion.
2010-09-01 | GSE21640 | GEO
Project description:This SuperSeries is composed of the following subset Series: GSE21640: Gene expression analysis of cardiomyocytes treated with a clinically relevant concentration of DEHP (50 ug/mL) GSE21641: Dose-dependent gene expression analysis of cardiomyocytes treated with DEHP (1-50 ug/mL) Refer to individual Series
2010-09-01 | E-GEOD-21642 | biostudies-arrayexpress
Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Experiment Overall Design: two condition experiment, Leydig cells from DEHP-treated mice vs. Leydig cells from vehicle-treated mice. Biological replicates: 2 DEHP-treated samples and 3 vehicle-treated samples. Each treated sample has been hybridized against each vehicle-treated sample in a dye-swap design. N=2 DEHP-treated x 3 vehicle-treated x 2 microarrays=12 microarrays
2009-04-10 | E-GEOD-13240 | biostudies-arrayexpress
Project description:BACKGROUND: Phthalates are manmade industrial additives used mostly as plasticizers. In addition to their deleterious effects on male genital development, population studies have recently documented correlations between phthalates exposure and subtle impacts on reproductive tract development and on the metabolic syndrome in male adults. In mature rodents liver di-(2-ethylhexyl)-phthalate (DEHP) activates the peroxisome proliferators-activated receptor (PPARalpha), a member of the nuclear receptor (NR) superfamily. OBJECTIVES: Using a systems biology approach, we aimed at defining potential mechanisms underlying the impacts of DEHP on adult mouse liver and testis. METHODS: Thus, we performed a parallel analysis of transcript and metabolic profiles in the liver from adult mice exposed to varying DEHP doses. Moreover, we obtained pangenomic mRNA profiles of laser-captured Leydig and Sertoli cells from mature animals exposed to DEHP. RESULTS: Hepatic genes modulated by DEHP are predominantly PPARalpha targets. However, the induction of some prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways. Integration of hepatic transcriptomic and metabonomic profiles further revealed a correlation between the impacts of DEHP on a cluster of genes and metabolites linked to heme synthesis and on a cluster of Rev-erbalpha target genes related to metabolic and circadian clock pathways. Cell-specific effects of DEHP were investigated in the adult testis and a noticeable impact of DEHP was observed on Leydig cells transcriptome. CONCLUSIONS: We report a detailed analysis of DEHP interference with hepatic Constitutive Androstane Receptor (CAR) and Rev-erbalpha pathways and a novel transcriptional impact of DEHP on adult endocrine cells of the testis. Experiment Overall Design: two condition experiment, Sertoli cells-rich areas from DEHP-treated mice vs. Sertoli cells-rich areas from vehicle-treated mice. Biological replicates: 4 DEHP-treated samples and 4 vehicle-treated samples. Dye-swap design. N=4 DEHP-treated vs vehicle-treated x 2 microarrays (dye-swap)=8 microarrays
2009-04-10 | E-GEOD-13237 | biostudies-arrayexpress
Project description:This SuperSeries is composed of the following subset Series:; GSE13237: Effect of DEHP on adult mouse Sertoli cells rich areas (SCRA); GSE13240: Effect of DEHP on adult mouse Leydig cells Experiment Overall Design: Refer to individual Series
2009-02-27 | E-GEOD-13241 | biostudies-arrayexpress
Project description:Role of PPARalpha in the effects of DEHP on the hepatic expression of a selection of mouse genes related to nuclear receptor signaling. Di-(2-ethylhexyl)-phthalate (DEHP), a widely used plasticizer, is detected in consumerâs body fluids. Contamination occurs through environmental and food chain sources. In mouse liver, DEHP activates the peroxisome proliferator-activated receptor alpha (PPARalpha) and regulates the expression of its target genes. Several in vitro investigations support the simultaneous recruitment of additional nuclear receptor pathways. We investigated, in vivo, the hepatic impact of low doses of DEHP on PPARalpha activation, and the putative activation of additional signalling pathways. Wild-type and PPARalpha-deficient mice were exposed to different doses of DEHP. Gene expression profiling delineated the role of PPARalpha and revealed a PPARalpha-independent regulation of several prototypic Constitutive Androstane Receptor (CAR) target genes. This finding demonstrates that CAR also represents a transcriptional regulator sensitive to phthalates. CAR-mediated effects of DEHP provide a new rationale for most endpoints of phthalates toxicity described previously, including endocrine disruption, hepatocarcinogenesis and the metabolic syndrome. Keywords: Treatment effect One-color macroarrays, 6 experimental conditions: Wild type (WT) and PPARalpha-deficient mice (PPAR) were treated with vehicle (Ctrl) or with di-(2-ethylhexyl)-phthalate (DEHP) at 20 mg/kg/day (D20) or 200 mg/kg/day (D200) for 21 days, Biological replicates: 10 for each group, One replicate per array
2010-05-22 | E-GEOD-14920 | biostudies-arrayexpress
Project description:Phthalates are industrial additives widely used as plasticizers. In addition to deleterious effects on male genital development, population studies have documented correlations between phthalates exposure and impacts on reproductive tract development and on the metabolic syndrome in male adults. In this study we investigated potential mechanisms underlying the impact of di-(2-ethylhexyl)-phthalate (DEHP) on adult mouse liver in vivo. A parallel analysis of hepatic transcript and metabolic profiles from adult mice exposed to varying DEHP doses was performed. Hepatic genes modulated by DEHP are predominantly PPARα targets. However, the induction of prototypic cytochrome P450 genes strongly supports the activation of additional NR pathways, including Constitutive Androstane Receptor (CAR). Integration of transcriptomic and metabonomic profiles revealed a correlation between the impacts of DEHP on genes and metabolites related to heme synthesis and on the Rev-erbα pathway that senses endogenous heme level. Keywords: Treatment effect One-color macroarrays, 4 experimental conditions: Control mice (vehicle treated), mice treated with di-(2-ethylhexyl)-phthalate (DEHP) at 30 mg/kg/day (D30), 180 mg/kg/day (D180) or 1100 mg/kg/day (D1100) for 14 days, Biological replicates: 6 controls, 4 D30, 4 D180, 5 D1100, One replicate per array
2010-05-05 | E-GEOD-14629 | biostudies-arrayexpress
Project description:Gene expression analysis was conducted on the wildtype Caenorhabditis elegans exposed to bisphenol A (BPA), di(2-ethylhexyl) phthalate (DEHP) and nonylphenol (NP) using whole genome microarray. The microarray study was conducted in an ecotoxicological context, by investigating the response of global gene expression with that of classical toxicological endpoints, such as, mortality, growth, reproduction and development. Results provide insight into global transcription response of C.elegans to these endocrine disrupting chemicals exposure and also contribute to enhance the potential of C.elegans microarray in ecotoxicology (ecotoxicogenomics). key word : ecotoxicogenomics Experiment Overall Design: Young adults of wildtype C.elegans from age-synchronized population were exposed to NP, DEHP and BPA at the concentrations equivalent to 1/100 of 24h LC50 of each chemical, for 24 h and RNA extraction and hybridization were subsequently conducted using C.elegans Genome array (Affymetrix).
2009-03-07 | E-GEOD-15016 | biostudies-arrayexpress