PUBLICATION

Epicardium Formation as a Sensor in Toxicology

Authors
Hofsteen, P., Plavicki, J., Peterson, R.E., Heideman, W.
ID
ZDB-PUB-140923-30
Date
2013
Source
Journal of developmental biology   1: 112-125 (Journal)
Registered Authors
Heideman, Warren, Peterson, Richard E., Plavicki, Jessica
Keywords
AHR, TCDD, epicardium, heart regeneration, proepicardium
MeSH Terms
none
PubMed
25232532 Full text @ J Dev Biol
Abstract
Zebrafish (Danio rerio) are an excellent vertebrate model for studying heart development, regeneration and cardiotoxicity. Zebrafish embryos exposed during the temporal window of epicardium development to the aryl hydrocarbon receptor (AHR) agonist 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) exhibit severe heart malformations. TCDD exposure prevents both proepicardial organ (PE) and epicardium development. Exposure later in development, after the epicardium has formed, does not produce cardiac toxicity. It is not until the adult zebrafish heart is stimulated to regenerate does TCDD again cause detrimental effects. TCDD exposure prior to ventricular resection prevents cardiac regeneration. It is likely that TCDD-induced inhibition of epicardium development and cardiac regeneration occur via a common mechanism. Here, we describe experiments that focus on the epicardium as a target and sensor of zebrafish heart toxicity.
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