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• Hofsteen, P
• Plavicki, J
• Peterson, RE.
• Heideman, W
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• Hofsteen, P
• Plavicki, J
• Peterson, RE.
• Heideman, W
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• Hofsteen, P
• Plavicki, J
• Peterson, RE.
• Heideman, W

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J. Dev. Biol. 2013, 1(2), 112-125; doi:10.3390/jdb1020112

Review

Epicardium Formation as a Sensor in Toxicology

Peter Hofsteen, Jessica Plavicki, Richard E. Peterson and Warren Heideman *

Department of Pharmaceutical Sciences, University of Wisconsin, 777 Highland Ave, Madison, WI 53705, USA

* Author to whom correspondence should be addressed.

Received: 27 May 2013; in revised form: 12 July 2013 / Accepted: 15 July 2013 / Published: 24 July 2013

(This article belongs to the Special Issue Epicardial Development and Cardiovascular Disease)

Download PDF Full-Text [184 KB, uploaded 24 July 2013 13:54 CEST]

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.

Keywords: epicardium; proepicardium; TCDD; AHR; heart regeneration

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