ArticleToxicological sciences : an official journal of the Society of Toxicology2010
Dioxin exposure disrupts the differentiation of mouse embryonic stem cells into cardiomyocytes.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 44 citations in OpenAlex.
- Predictive biomarkers for embryotoxicity: a machine learning approach to mitigating multicollinearity in RNA-Seq.Archives of toxicology · 2024Article
- A new approach to study stochastic epigenetic mutations in sperm methylome of Vietnam war veterans directly exposed to Agent Orange.Environmental epigenetics · 2024Article
- TCDD alters essential transcriptional regulators of osteogenic differentiation in multipotent mesenchymal stem cells.Toxicological sciences : an official journal of the Society of Toxicology · 2023Article
- A review of food contaminant 2,3,7,8-tetrachlorodibenzo-p-dioxin and its toxicity associated with metabolic disorders.Current research in food science · 2023Review
- Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Impact of AHR Ligand TCDD on Human Embryonic Stem Cells and Early Differentiation.International journal of molecular sciences · 2020Article
- Aryl Hydrocarbon Receptor (AHR) Ligands as Selective AHR Modulators (SAhRMs).International journal of molecular sciences · 2020Review
- Ah receptor ligands and their impacts on gut resilience: structure-activity effects.Critical reviews in toxicology · 2020Review
- 2,4-D causes oxidative stress induction and apoptosis in human dental pulp stem cells (hDPSCs).Environmental science and pollution research international · 2019Article
- Evidence for Aryl hydrocarbon Receptor-Mediated Inhibition of Osteoblast Differentiation in Human Mesenchymal Stem Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2019Article
- SERPINB2 is a novel indicator of stem cell toxicity.Cell death & disease · 2018Article
- Aryl Hydrocarbon Receptor Ablation in Cardiomyocytes Protects Male Mice From Heart Dysfunction Induced by NKX2.5 Haploinsufficiency.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Ah Receptor Activation by Dioxin Disrupts Activin, BMP, and WNT Signals During the Early Differentiation of Mouse Embryonic Stem Cells and Inhibits Cardiomyocyte Functions.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Role of Hox genes in stem cell differentiation.World journal of stem cells · 2015Review
- Sex- and tissue-specific methylome changes in brains of mice perinatally exposed to lead.Neurotoxicology · 2015Article
- Actions of endocrine-disrupting chemicals on stem/progenitor cells during development and disease.Endocrine-related cancer · 2014Review
- Role of the aryl hydrocarbon receptor in carcinogenesis and potential as a drug target.Toxicological sciences : an official journal of the Society of Toxicology · 2013Review
- Article
- Inhibition of cytochrome P4501-dependent clearance of the endogenous agonist FICZ as a mechanism for activation of the aryl hydrocarbon receptor.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Genetic architecture of susceptibility to PCB126-induced developmental cardiotoxicity in zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2011Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Experimental exposure of fish, birds, and rodents to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD; dioxin) causes multiple Ah receptor-mediated developmental abnormalities, an observation consistent with compelling evidence in human populations that TCDD exposure is responsible for a significant incidence of birth defects. To characterize molecular mechanisms that might explain the developmental effects of dioxin, we have studied the consequences of TCDD exposure on the differentiation of mouse embryonic stem (ES) cells in culture and on the expression of genes, including those coding for homeodomain containing transcription factors, with a role in progression of tissue differentiation and embryonic identity during development. We find that TCDD treatment causes expression changes in a number of homeobox genes concomitant with Ah receptor recruitment to the promoters of many of these genes, whether under naïve or dioxin-activated conditions. TCDD exposure also derails temporal expression trajectories of developmentally regulated genes in a wide diversity of differentiation pathways, including genes with functions in neural and cardiovascular development, self-renewal, hematopoiesis and mesenchymal lineage specification, and Notch and Wnt pathways. Among these, we find that TCDD represses the expression of the cardiac development-specific Nkx2.5 homeobox transcription factor, of cardiac troponin-T and of alpha- and beta-myosin heavy chains, inhibiting the formation of beating cardiomyocytes, a characteristic phenotype of differentiating mouse ES cells in culture. These data identify potential pathways for dioxin to act as a developmental teratogen, possibly critical to cardiovascular development and disease, and provide molecular targets that may help us understand the molecular basis of Ah receptor-mediated developmental toxicity.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.