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Transcriptomic effects of mono-(2-ethylhexyl) phthalate and all-trans retinoic acid in the cultured mouse fetal testes

ABSTRACT: We report the results of an RNA-seq analysis conducted as part of an experiment investigating the effects of the phthalate, mono-(2-ethylhexyl) phthalate (MEHP), and all-trans retinoic acid (ATRA) on cultured fetal mouse testes. The goal of the study was to determine whether fetal testis toxicity of MEHP is partially driven by disruption of retinoic acid signaling.

ORGANISM(S): Mus musculus

PROVIDER: GSE195969 | GEO | 2022/02/05

REPOSITORIES: GEO

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Transcriptomic alterations induced by physiologically relevant level of mono(2-ethylhexyl) phthalate (MEHP) in oocytes and blastocysts

Project description:Mono(2-ethylhexyl) phthalate (MEHP), the main di(2-ethylhexyl) phthalate (DEHP) metabolite, is a known reproductive toxicant. Residual levels of 20 nM MEHP have been found in follicular fluid aspirated from IVF-treated women and DEHP-treated animals. It is not yet clear whether these residual MEHP levels have any effect on the follicle-enclosed oocyte or developing embryo. To clarify this point, bovine oocytes were matured with or without 20 nM MEHP for 22 h. Microarray analysis was performed for both mature oocytes and 7-day blastocysts. A feasibility examination was performed on mature oocytes (n = 200/group) to reveal a possible direct effect on the oocyte proteomic profile. Transcriptome analysis revealed MEHP-induced alterations in the expression of 456 and 290 genes in oocytes and blastocysts, respectively. The differentially expressed genes are known to be involved in various biological pathways, such as transcription process, cytoskeleton regulation and metabolic pathway. Among these, the expression of 9 genes was impaired in both oocytes exposed to MEHP (i.e., direct effect) and blastocysts developed from those oocytes (i.e., carryover effect). In addition, 191 proteins were found to be affected by MEHP in mature oocytes. The study explores, for the first time, the risk associated with exposing oocytes to physiologically relevant MEHP concentrations to the maternal transcripts. Although it was the oocytes that were exposed to MEHP, alterations carried over to the blastocyst stage, following embryonic genome activation, implying that these embryos are of low quality.

2019-05-09 | PXD012092 | Pride

Mono(2-ethylhexyl) phthalate induces transcriptomic changes in placental cells based on concentration, fetal sex, and trophoblast cell type

Project description:Phthalates are ubiquitous plasticizer chemicals found in consumer products. Exposure to phthalates during pregnancy has been associated with adverse pregnancy and birth outcomes and differences in placental gene expression in human studies. The objective of this research was to evaluate global changes in placental gene expression via RNA sequencing in two placental cell models following exposure to the phthalate metabolite mono(2-ethylhexyl) phthalate (MEHP). HTR-8/SVneo and primary syncytiotrophoblast cells were exposed to three concentrations (1, 90, 180µM) of MEHP for 24 hours with DMSO (0.1%) as a vehicle control. mRNA and lncRNAs were quantified using paired end RNA sequencing, followed by identification of differentially expressed genes (DEGs) and significant KEGG pathways and enriched transcription factors (TFs). MEHP caused gene expression changes across all concentrations for HTR-8/SVneo and primary syncytiotrophoblast cells. Sex-stratified analysis of primary cells identified different patterns of sensitivity in response to MEHP dose by sex, with male placentas being more responsive to MEHP exposure. Pathway analysis identified 11 KEGG pathways significantly associated with at least one concentration in both cell types. Four ligand-inducible nuclear hormone TFs (PPARG, PPARD, ESR1, AR) were enriched in at least three treatment groups. Overall, we demonstrated that MEHP differentially affects placental gene expression based on concentration, fetal sex, and trophoblast cell type. This study confirms prior studies as enrichment of nuclear hormone TFs were concordant with previously published mechanisms of phthalate disruption, and generates new hypotheses, as we identified many pathways and genes not previously linked to phthalate exposure.

2023-05-01 | GSE217210 | GEO

Toxicogenomic Screen of Replacements for bis(2-ethylhexyl) phthalate (DEHP) Using the Immortalized TM4 Sertoli Cell Line

Project description:Phthalate plasticizers are being phased out of consumer products because of their endocrine disrupting properties. This has resulted in a need to find safe alternatives that can plasticize polyvinyl chloride (PVC) while being inexpensive and biodegradable. We aim to study the toxicogenomic profile of mono-(2-ethylhexyl) phthalate (MEHP, the active metabolite of bis(2-ethylhexyl) phthalate, DEHP), the commercial plasticizer 1,2-cyclohexane dicarboxylic acid diisononyl ester (DINCH), and three plasticizers in development (1,4 butanediol dibenzoate (BDB), dioctyl succinate (DOS), and dioctyl maleate (DOM)) using the immortalized TM4 Sertoli cell line.

2015-08-06 | GSE66812 | GEO

Toxicogenomic Screen of Replacements for bis(2-ethylhexyl) phthalate (DEHP) Using the Immortalized TM4 Sertoli Cell Line

2015-08-06 | E-GEOD-66812 | biostudies-arrayexpress

Transcription profiling of rat testes following exposure to mono-(2-ethylhexyl) phthalate

Project description:In rodent models, phthalate exposure alters both the fetal and pubertal testis, but the resulting histopathological changes are divergent. This suggests that the underlying molecular and cellular phthalate mechanism may be age-dependent. Using genome-wide expression profiling of acutely-exposed rats, the initial molecular response in pubertal rat testis following in vivo phthalate exposure was determined. For this study, postnatal day 28 rats were exposed to a single dose of 1 g/kg mono-(2-ethyl)hexyl phthalate (MEHP) and assayed at 1, 2, 3, 6, and 12 hrs thereafter using Affymetrix Rat Genome 230 2.0 Arrays. Experiment Overall Design: At each timepoint, testes from 3 treated and 3 control (corn oil gavage) were analzyed.

2007-11-06 | E-GEOD-4514 | biostudies-arrayexpress

DNA Methylation and Transcriptomic Profiles of Early Organogenesis-Stage Mouse Conceptuses after Exposure to Mono-2-Ethylhexyl Phthalate: Effects in the Absence and Presence of Neural Tube Defects

Project description:The goal of this study was to assess changes in gene expression and DNA methylation in response to embryonic exposures to the plasticizer metabolite, mono-2-ethylhexyl phthalate (MEHP). Because we previously observed increased incidence of neural tube defects (NTDs) in exposed embryos, we also stratified our samples by NTD status to examine changes in expression or methylation that may be associated with NTD progression in response to MEHP.

2024-07-31 | GSE180254 | GEO

DNA Methylation Profiles of Early Organogenesis-Stage Mouse Conceptuses after Exposure to Mono-2-Ethylhexyl Phthalate: Effects in the Absence and Presence of Neural Tube Defects

Project description:The goal of this study was to assess whether changes in DNA methylation were observed following MEHP treatment in mouse embryos. Explanted GD8 mouse embryos were exposed to 100 ug/ml mono-2-ethylhexyl phthalate (MEHP) or dimethyl sulfoxide (0.01%; control) in whole embryo culture for 24 h. On GD9 tissues were manually separated using watchmaker's forceps and placed for genomic DNA isolation. At that time, the presennce (positive) or absence (negative) of a neural tube defect in the mouse embryos was noted.

2024-07-31 | GSE180608 | GEO

Expression data from HeLa cell treated with Bisphenol S and Mono-ethylhexyl phthalate

Project description:Bisphenol S and mono-ethylhexyl phthalate are widely used in the industry of making plastic, mailing envelopes, tickets, etc. Humans are exposed to these compounds by skin contact, inhalation, and food ingestions. However, the molecular mechanisms of these compounds' adverse effects are still unclear. We address the molecular and cellular mechanisms underlying Bisphenol S and mono-ethylhexyl phthalate effects on HeLa cells. Here microarray analysis was performed to identify distinct classes of up- or down-regulated genes and their connections to the different metabolic pathways.

2020-05-27 | GSE147533 | GEO

Toxicoproteomics of environmental mixtures in prostate diseases

Project description:These data are from the following 2 experiments: 1. normal prostate stromal cells (BHPRS1) treated with either 0.1 uM mono(2-ethylhexyl) phthalate (MEHP), 3 uM perfluorooctanesulfonic acid (PFOS), the mixture of MEHP+PFOS, or DMSO vehicle (0.06% v/v); n=3 each 2. metastatic prostate epithelial cells (MT10) treated with 50 uM mono(2-ethylhexyl) phthalate (MEHP) or DMSO vehicle (0.06% v/v); n=4 each

2024-05-21 | PXD014428 | Pride

Differential DNA methylation at conserved non-genic elements and transgenerational inheritance following developmental exposure to mono(2-ethylhexyl) phthalate and 5-azacytidine in zebrafish

Project description:Background Exposure to environmental stressors during development may lead to latent and transgenerational adverse health effects. To understand the role of DNA methylation in these effects, we used zebrafish as a vertebrate model to investigate heritable changes in DNA methylation following chemical induced stress during early development. We exposed zebrafish embryos to non-embryotoxic concentrations of the biologically active phthalate metabolite mono-(2-ethylhexyl) phthalate (MEHP, 30 µM), and the DNA methyltransferase 1 inhibitor 5-azacytidine (5AC, 10 µM). Direct, latent and transgenerational effects on DNA methylation were assessed using global, genome wide and locus specific DNA methylation analyses. Results Following direct exposure in zebrafish embryos from 0 to 6 days post fertilization (dpf), genome wide analysis revealed a multitude of differentially methylated regions, strongly enriched at conserved non-genic elements for both compounds. Pathways involved in adipogenesis were enriched with the putative obesogenic compound MEHP. Exposure to 5AC resulted in enrichment of pathways involved in embryonic development, and transgenerational effects on larval body length. Locus specific methylation analysis of 10 differentially methylated sites revealed six of these loci differentially methylated in sperm sampled from adult zebrafish exposed during development to 5AC, and in first and second generation larvae. With MEHP consistent changes were found at 2 specific loci in first and second generation larvae. Conclusions Our results suggest a functional role for DNA methylation on cis-regulatory conserved elements following developmental exposure to compounds. Effects on these regions are potentially transferred to subsequent generations.

2017-03-09 | GSE84736 | GEO

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