ArticleToxicological sciences : an official journal of the Society of Toxicology2013
Dioxin inhibits zebrafish epicardium and proepicardium development.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 46 citations in OpenAlex.
- An Overview of Adverse Outcome Pathway Links between PMEnvironment & health (Washington, D.C.) · 2024Review
- Effects of Hudson River Stressors on Atlantic Tomcod: Contaminants and a Warming Environment.Reviews in fisheries science & aquaculture · 2023Article
- Environmentally relevant uptake, elimination, and metabolic changes following early embryonic exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin in zebrafish.Chemosphere · 2023Article
- Proper modulation of AHR signaling is necessary for establishing neural connectivity and oligodendrocyte precursor cell development in the embryonic zebrafish brain.Frontiers in molecular neuroscience · 2022Article
- Developmental and lifelong dioxin exposure induces measurable changes in cardiac structure and function in adulthood.Scientific reports · 2021Article
- Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Casting a wide net: use of diverse model organisms to advance toxicology.Disease models & mechanisms · 2020Article
- Mechanisms of Developmental Toxicity of Dioxins and Related Compounds.International journal of molecular sciences · 2019Review
- sox9b is required in cardiomyocytes for cardiac morphogenesis and function.Scientific reports · 2018Article
- TCF21 and the environmental sensor aryl-hydrocarbon receptor cooperate to activate a pro-inflammatory gene expression program in coronary artery smooth muscle cells.PLoS genetics · 2017Article
- More than Just a Simple Cardiac Envelope; Cellular Contributions of the Epicardium.Frontiers in cell and developmental biology · 2017Review
- Mechanistic Evaluation of Benzo[a]pyrene's Developmental Toxicities Mediated by Reduced Cyp19a1b Activity.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
- Quantitative proteomics identify DAB2 as a cardiac developmental regulator that inhibits WNT/β-catenin signaling.Proceedings of the National Academy of Sciences of the United States of America · 2016Article
- Dioxin disrupts cranial cartilage and dermal bone development in zebrafish larvae.Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- Dioxin inhibition of swim bladder development in zebrafish: is it secondary to heart failure?Aquatic toxicology (Amsterdam, Netherlands) · 2015Article
- Cardiac development in zebrafish and human embryonic stem cells is inhibited by exposure to tobacco cigarettes and e-cigarettes.PloS one · 2015Article
- Intersection of AHR and Wnt signaling in development, health, and disease.International journal of molecular sciences · 2014Review
- Zebrafish: A marvel of high-throughput biology for 21Current environmental health reports · 2014Article
- Cardiac myocyte-specific AHR activation phenocopies TCDD-induced toxicity in zebrafish.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Embryonic exposure to the environmental contaminant and aryl hydrocarbon receptor agonist, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, dioxin), disrupts cardiac development and function in fish, birds, and mammals. In zebrafish, the temporal window of sensitivity to the cardiotoxic effects of TCDD coincides with epicardium formation. We hypothesized that this TCDD-induced heart failure results from disruption of epicardial development. To determine whether embryonic TCDD exposure inhibits epicardium and proepicardium (PE) development in zebrafish, we used histology and fluorescence immunocytochemistry to examine the epicardium formation in fish exposed to TCDD. TCDD exposure prevented epicardium formation. Using live imaging and in situ hybridization, we found that TCDD exposure blocked the formation of the PE cluster. In situ hybridization experiments showed that TCDD exposure also prevented the expression of the PE marker tcf21 at the site where the PE normally forms. TCDD also inhibited expansion of the epicardial layer across the developing heart: Exposure after PE formation was completed prevented further expansion of the epicardium. However, TCDD exposure did not affect epicardial cells already present. Because TCDD blocks epicardium formation, but is not directly toxic to the epicardium once complete, we propose that inhibition of epicardium formation can account for the window of sensitivity to TCDD cardiotoxicity in developing zebrafish. Epicardium development is crucial to heart development. Loss of this layer during development may account for most if not all of the TCDD-induced cardiotoxicity in zebrafish.
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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.