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Evaluation of differential gene expression in a placental cell line exposed to the trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine (DCVC)

ABSTRACT: Trichloroethylene (TCE) is an industrial solvent and widespread environmental contaminant. Human TCE exposure is prevalent, though epidemiological studies testing TCE exposure and adverse birth outcomes are inconclusive. The TCE metabolite S-(1,2-dichlorovinyl)-L-cysteine (DCVC) exhibits toxicity at human-relevant concentrations in a placental cell line. To date, DCVC cytotoxicity mechanistic studies have been limited to single molecular signaling pathways and biological responses. In the current study, genome-wide gene expression and gene set enrichment analyses (GSEA) were used to identify novel genes and pathways altered by human exposure-relevant DCVC concentrations in the human placental cell line HTR-8/SVneo. The results of this study were compared to a parallel study using placental villous exlant tissues.

ORGANISM(S): Homo sapiens

PROVIDER: GSE154339 | GEO | 2021/03/16

REPOSITORIES: GEO

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Evaluation of differential gene expression in placental tissues exposed to the trichloroethylene metabolite S-(1,2-dichlorovinyl)-L-cysteine (DCVC)

Project description:Trichloroethylene (TCE) is an industrial solvent and widespread environmental contaminant. Human TCE exposure is prevalent, though epidemiological studies testing TCE exposure and adverse birth outcomes are inconclusive. The TCE metabolite S-(1,2-dichlorovinyl)-L-cysteine (DCVC) exhibits toxicity at human-relevant concentrations in a placental cell line. To date, DCVC cytotoxicity mechanistic studies have been limited to single molecular signaling pathways and biological responses. In the current study, genome-wide gene expression and gene set enrichment analyses (GSEA) were used to identify novel genes and pathways altered by human exposure-relevant DCVC concentrations in human placental villous explant tissues. The results of this study were compared to a parallel study using the placental cell line HTR-8/SVneo.

2021-03-16 | GSE154489 | GEO

Trichloroethylene-induced mRNA expression changes in B6C3F1 mouse liver

Project description:To examine changes, if any, in the expression of mRNAs in the liver tissue of mice, we have employed whole genome microarray expression profiling as a discovery platform to identify genes responsive to Trichloroethylene (TCE) treatment. In our results, the expression levels of 431 mRNAs were changed after TCE exposure, of which 291 were up-regulated and 140 were down-regulated. Using qPCR, we validated six of the mRNA expression changed genes, viz., Jun, Cdkn1a, Rad51b, Uhrf1, Svil and Ihh. Six B6C3F1 male mice were oral administrated with either corn oil or TCE (dissolved in corn oil, 1000mg/kg b.w per day) for 5 days. The expression changes of mRNAs in TCE exposured mouse liver were screened by whole genome microarray expression profiling and were validated by qPCR.

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Transcriptional responses to maternal trichloroethylene and/or N-acetyl cysteine exposure in Wistar rat placental tissue

Project description:Trichloroethylene (TCE) is a persistent and pervasive environmental contaminant. N-acetyl cysteine (NAC) is an antioxidant that may reduce TCE effects. Pregnant Wistar rats were exposed to 480 mg TCE mg/kg/day, 200 mg/kg/day NAC or co-exposure with both chemicals via ingestion (mini vanilla wafer) on gestation days 6-16 (tissue collection day). TCE- and/or NAC-induced changes to gene expression were evaluated in male and female rat placentae.

2022-06-01 | GSE168232 | GEO

Trichloroethylene-induced mRNA expression changes in B6C3F1 mouse liver

2014-11-14 | GSE58819 | GEO

The trichloroethylene metabolite S-(1,2-dichlorovinyl)-l-cysteine inhibits lipopolysaccharide-induced inflammation transcriptomic pathways and cytokine secretion in a macrophage cell model

Project description:Macrophage cells play a critical role in the innate immune response during infection. Previous studies have reported that the trichloroethylene (TCE) metabolite S-(1,2-dichlorovinyl)-l-cysteine (DCVC) inhibits cytokine secretion in pathogen stimulated placental membranes, but little is known about the mechanism for these effects, including which cell types or transcriptomic pathways are impacted. We tested the hypothesis that DCVC inhibits lipopolysaccharide (LPS) stimulated inflammation pathways in differentiated (macrophage like) THP-1 cells. THP-1 cells were differentiated with phorbol 12-myristate 13-acetone (PMA) for 24 h and then treated with 1, 5, or 10 µM DCVC for 24 h. After an additional 4 h incubation with lipopolysaccharide (LPS), RNA was harvested, and RNA sequencing and cytokine analysis was performed. There were 1,399 differentially expressed genes in the cells co-treated with DCVC and LPS compared to LPS alone. Major pathways impacted include the inflammatory response, response to cytokines, and leukocyte activation. Finally, DCVC significantly reduced LPS-stimulated IL-1β, IL-6, and TNF-α secretion. These findings suggest that TCE could potentially modify important macrophage functions during infection.

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The effect of trichloroethylene on gene expression in mouse liver

Project description:Trichloroethylene (TCE) is a widely used industrial chemical, and a common environmental contaminant. It is a well-known carcinogen in rodents and a probable carcinogen in humans. Studies utilizing panels of mouse inbred strains afford a unique opportunity to understand both metabolic and genetic basis for differences in responses to TCE. We tested the hypothesis that individual and liver-specific toxic effects of TCE are genetically controlled and that the mechanisms of toxicity and susceptibility can be uncovered by exploring responses to TCE using a diverse panel of inbred mouse strains. TCE (2100 mg/kg) or corn oil vehicle were administered by gavage to 6-8 wk old male mice of 15 mouse strains. Serum and liver were collected at 2, 8, and 24 hr post dosing and were analyzed for TCE metabolites, hepatocellular injury and gene expression of liver. TCE metabolism, as evident from the levels of individual oxidative and conjugative metabolites, varied considerably between strains. TCE treatment-specific effect on the liver transcriptome was strongly dependent on the individual’s genetic background. PPAR-mediated molecular networks, consisting of the metabolism genes known to be induced by TCE, represent some of the most pronounced molecular effects of TCE treatment in mouse liver that are dependent on the individual’s genetic background. Conversely, cell death, liver necrosis, and immune mediated response pathways which are affected by TCE treatment in liver are largely genetic background-independent. These studies provide better understanding of the mechanisms of TCE-induced toxicity anchored on metabolism and genotype-phenotype correlations that may define susceptibility or resistance. 16 mouse strains were studied, vehicle control and mice treated by gavage with 2100 mg/kg Trichloroethylene and sacrificed 24 hrs after dosing

2011-02-01 | E-GEOD-24278 | biostudies-arrayexpress

Mitochondrial dysfunction, disruption of F-actin polymerization, and transcriptomic alterations in zebrafish larvae exposed to trichloroethylene

Project description:Trichloroethylene (TCE) is primarily used as an industrial degreasing agent and has been in use since the 1940s. TCE is released into the soil, surface, and groundwater. From an environmental and regulatory standpoint more than half of Superfund hazardous waste sites on the National Priority List are contaminated with TCE. Occupational exposure to TCE occurs primarily via inhalation, while environmental TCE exposure also occurs through ingestion of contaminated drinking water. Current literature links TCE exposure to various adverse health effects including cardiovascular toxicity. Current studies aiming to address developmental cardiovascular toxicity utilized rodent and avian models with the majority of studies using relatively higher parts per million (ppm; mg/L) doses. In this study to further investigate developmental cardiotoxicity of TCE, zebrafish embryos were treated with 0, 10, 100, or 500 parts per billion (ppb; μg/L) TCE during embryogenesis and/or through early larval stages. After the appropriate exposure period, angiogenesis, F-actin polymerization, and mitochondrial function were assessed. A significant dose response decrease in angiogenesis, F-actin polymerization, and mitochondrial function was observed. To further complement this data, a transcriptomic profile of zebrafish larvae was completed to identify gene alterations associated with the 10 ppb TCE exposure. Results from the transcriptomic data revealed that an embryonic TCE exposure caused significant changes in genes associated with cardiovascular disease, cancer, and organismal injury and abnormalities with a number of targets in the FAK signaling pathway. Overall, results from our study further support TCE as a developmental cardiovascular toxicant and continued priority for environmental regulation.

2016-02-01 | GSE72918 | GEO

Mechanism of Trichloroethylene (TCE) toxicity in the placenta

Project description:Cells in culture will be exposed to S-(1,2-dichlorovinyl)-L-cysteine (DCVC), a relevant metabolite of TCE. The first cell line used will be HTR-8/SVneo, originally derived from first trimester female human cytotrophoblast cells and immortalized with simian virus 40 large T antigen, this cell line models first-trimester placental extravillous trophoblasts in vitro. HTR-8/SVneo cells will be cultured for 24 hours followed by exposure to cell culture media (control) or 20 µM DCVC for 6 or 12 hours. Cells (cells frozen in cell culture dish) will then be collected (n=5) In the TCE aim of this study, we will utilize one cell model that phenotypically represents an important placental cell population.

2020-06-08 | ST001398 | MetabolomicsWorkbench

Trichloroethylene-induced miRNA expression changes in B6C3F1 mouse liver

Project description:To know if Trichloroethylene (TCE) can induce miRNA expression changes in mouse liver, we use microarray to screen for differentially expressed miRNAs in the liver of mice exposed to TCE at a dose of 1000 mg/kg b.w. for 5days . In our results, nine miRNAs were selected by volcano plot filtering (fold change ≥ 2 and P-value ≤ 0.05), out of which eight were up-regulated and one was down-regulated. The differential expression of miR-182-5p, miR-34a-5p and miR-451a were validated by qPCR.

2016-11-22 | GSE85904 | GEO

Comparative dose-response analysis of liver and kidney transcriptomic effects of trichloroethylene and tetrachloroethylene in B6C3F1 mouse

Project description:Purpose: Trichloroethylene (TCE) and tetrachloroethylene (PCE) are ubiquitous environmental contaminants and occupational health hazards. The goals of this study were to establish the common and differing transcriptional effects of TCE and PCE. This study examined liver and kidney effects of TCE and PCE in a dose-response study design. Methods: Equi-molar doses of TCE (24, 80, 240, 800 mg/kg) or PE (30, 100, 300, 1,000 mg/kg) were administered by gavage in aqueous vehicle to male B6C3F1/J mice. Tissues were collected 24 hrs after exposure. Trichloroacetic acid (TCA), a major oxidative metabolite of both compounds, was measured and RNA sequencing was performed on liver and kidney samples, with ~30 samples for each organ (29 after QC). Results: Most dose-responsive pathways were common among chemicals/tissues, with the strongest effect on peroxisomal beta-oxidation. Effects on liver and kidney mitochondria-related pathways were notably unique to PCE. Tissue-specific acute transcriptional effects of TCE and PCE occurred at human equivalent doses comparable to those for apical effects. Conclusions: Our study is the first RNA-Seq transcriptional study of TCE vs. PCE in both liver and kidney, enabling a detailed comparison of the chemicals and effects on different organs. Our results show strong commonalities of effects, although PCE shows stronger transcriptional responses than TCE for the same equimolar doses.

2017-07-06 | GSE100296 | GEO

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