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Methylomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts

ABSTRACT: Methylomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts

PROVIDER: PRJNA474828 | ENA |

REPOSITORIES: ENA

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Methylomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts

Project description:CpG methylomic characterization of BDE-47 exposed cultured primary human cytrophoblasts (2nd trimester) undergoing differentiation in vitro.

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Transcriptomic analysis of HepG2 cells treated with BDE-47, BDE-99, BDE-209 and their ternary mixture at 1nM as a dietary relevant concentration

Project description:Polybrominated diphenyl ethers (PBDEs) are persistent organic chemicals implied as flame re-tardants. Humans are mainly exposed to BDE-47, -99 and -209 congeners by diet. PBDEs are metabolic disruptors with liver as main target organ. To investigate their mode of action at a human relevant concentration, we exposed HepG2 cells to these congeners and their mixture at 1 nM for 72h, analyzing their transcriptomic and proteomic profiles. KEGG pathways and GSEA Hallmarks enrichment analyses evidenced that BDE-47 disrupted the glucose metabolism and Hypoxia pathway; all the congeners and the MIX affected lipid metabolism and signaling Hallmarks regulating metabolism as mTORC1 and PI3K/AKT/MTOR. These results were confirmed by glucose secretion depletion and increased lipid accumulation, especially in BDE-47 and -209 treated cells. These congeners also affected the EGFR/MAPK signaling; further, BDE-47 enriched the Estrogen pathway. Interestingly, BDE-209 and the MIX increased ERα gene expression, whereas all the congeners and the MIX induced ERβ and PPARγ. We also found that PBDEs modulated several lncRNAs and that HNRNAP1 represented a central hub in all the four interaction networks. Overall, despite the low concentration used, the PBDEs investigated affected glucose and lipid metabolism with different underlying modes of action, as highlighted by the integrated omics analysis. These results may support the mechanism-based risk assessment of these compounds in relation to liver metabolism disruption.

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BDE-47 CpG Methylomic Alterations in Human Embryonic Stem Cell-derived Neural Precursor Cells

Project description:BDE-47 CpG Methylomic Alterations in Human Embryonic Stem Cell-derived Neural Precursor Cells

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Transcriptome profiling analysis of Mactra veneriformis exposed to BDE-47 by deep sequencing

Project description:RNA-seq provided a general overview of the gene expression profiles of the digestive glands of Mactra veneriformis exposed to 2, 2′,4,4′-tetrabromodiphenyl ether (BDE-47, a type of widely used brominated flame retardants).

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Toxicogenomic analysis of the effects of BDE-47/209, TBBPA/S, TCBPA on early neural development, with human embryonic stem cells

Project description:Flame retardants are detected globally in the environment, and pose great risks to human health. The potential effects of these chemicals on the development of nervous system have raise public concerns. In this study, to explore the toxicity profiles of these chemicals in the early developmental stage of human nervous system, we induced neural ectoderm from human embryonic stem cells in the presence of individual or mixture of BDE-47, BDE-209, TBBPA, TBBPS, TCBPA. By analyzing the whole transcriptional changes in the samples treated with 1 μΜ of each chemical, we identified a set of neural development relative biological processes that response to these chemicals. Genes involved in the GO terms relative to neural development were further confirmed by qRT-PCR assay, with samples treated with various concentrations (10 nM, 100 nM, 1 μΜ, 5 μΜ) of these chemicals. We found out that axon guidance and synaptogenesis may be the major target of these chemicals. In addition, these flame retardants may dysregulate the WNT and AHR signaling pathways. BDE-209 showed similar toxicity with BDE-47, whereas TBBPS and TCBPA may not be safe alternatives to TBBPA.

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Transcriptomic Analysis of Gonadal Adipose Tissue in Male Mice Exposed Perinatally to 2,2',4,4'- Tetrabromodiphenyl Ether (BDE-47)

Project description:For the majority of lipophilic compounds adipose tissue is traditionally considered as storage depot and only rarely as a target organ. Meanwhile, abnormalities in adipose tissue physiology induced by chemical exposures may contribute to the current epidemic of obesity and metabolic diseases. Polybrominated diphenyl ethers (PBDEs) is a group of lipophilic flame retardants found in majority of human samples in North America. Their ability to alter physiology of adipose tissue is unknown. We exposed pregnant mice to 0.2 mg/kg body weight/day of BDE-47 perinatally. Transcriptomic changes in gonadal adipose tissue were analyzed in male offspring using RNA-seq approach with subsequent bioinformatic analysis. Genes of coagulation and complement cascade, de novo lipogenesis, and xenobiotic metabolism were altered in expression in response to BDE-47 exposure. The affected molecular network included the following hubs: PPARα, HNF1A and HNF4. These findings suggest that adipose tissue should be considered a target tissue for BDE-47, in addition to its role as a storage depot. This study also builds a background for a targeted search of sensitive phenotypic endpoints of BDE-47 exposure, including lipid profile parameters and coagulation factors in circulation. Additional studies are needed to investigate the role of PBDEs as an obesogen.

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Genomic Profiling of BDE-47 Effects on Human Placental Cytotrophoblasts.

Project description:Despite gradual legislative efforts to phase out flame retardants (FRs) from the marketplace, polybrominated diphenyl ethers (PBDEs) are still widely detected in human maternal and fetal tissues, eg, placenta, due to their continued global application in consumer goods and inherent biological persistence. Recent studies in rodents and human placental cell lines suggest that PBDEs directly cause placental toxicity. During pregnancy, trophoblasts play key roles in uterine invasion, vascular remodeling, and anchoring of the placenta-fetal unit to the mother. Thus, to study the potential consequences of PBDE exposures on human placental development, we used an in vitro model: primary villous cytotrophoblasts (CTBs). Following exposures, the endpoints that were evaluated included cytotoxicity, function (migration, invasion), the transcriptome, and the methylome. In a concentration-dependent manner, common PBDE congeners, BDE-47 and -99, significantly reduced cell viability and increased death. Upon exposures to sub-cytotoxic concentrations (≤ 5 µM), we observed BDE-47 accumulation in CTBs with limited evidence of metabolism. At a functional level, BDE-47 hindered the ability of CTBs to migrate and invade. Transcriptomic analyses of BDE-47 effects suggested concentration-dependent changes in gene expression, involving stress pathways, eg, inflammation and lipid/cholesterol metabolism as well as processes underlying trophoblast fate, eg, differentiation, migration, and vascular morphogenesis. In parallel assessments, BDE-47 induced low-level global increases in methylation of CpG islands, including a subset that were proximal to genes with roles in cell adhesion/migration. Thus, using a primary human CTB model, we showed that PBDEs induced alterations at cellular and molecular levels, which could adversely impact placental development.

| S-EPMC6317432 | biostudies-literature

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