Epicardium Formation as a Sensor in Toxicology
Department of Pharmaceutical Sciences, University of Wisconsin, 777 Highland Ave, Madison, WI 53705, USA
*
Author to whom correspondence should be addressed.
J. Dev. Biol. 2013, 1(2), 112-125; https://doi.org/10.3390/jdb1020112
Received: 27 May 2013 / Revised: 12 July 2013 / Accepted: 15 July 2013 / Published: 24 July 2013
(This article belongs to the Special Issue Epicardial Development and Cardiovascular Disease)
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. View Full-TextKeywords:
epicardium; proepicardium; TCDD; AHR; heart regeneration
▼
Figures
Figure 1
This is an open access article distributed under the Creative Commons Attribution License (CC BY 3.0).
Share & Cite This Article
MDPI and ACS Style
Hofsteen, P.; Plavicki, J.; Peterson, R.E.; Heideman, W. Epicardium Formation as a Sensor in Toxicology. J. Dev. Biol. 2013, 1, 112-125.
Related Articles
Article Metrics
Comments
[Return to top]
J. Dev. Biol.
EISSN 2221-3759
Published by MDPI AG, Basel, Switzerland
RSS
E-Mail Table of Contents Alert