Epicardium Formation as a Sensor in Toxicology

Journal of Developmental Biology

Peter Hofsteen¹  Jessica Plavicki¹  Richard E. Peterson¹ 

[1] Department of Pharmaceutical Sciences, University of Wisconsin, 777 Highland Ave, Madison, WI 53705, USA;

关键词: epicardium;    proepicardium;    TCDD;    AHR;    heart regeneration;   

DOI  :  10.3390/jdb1020112

来源: mdpi

【 摘 要 】

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.

【 授权许可】

CC BY   
© 2013 by the authors; licensee MDPI, Basel, Switzerland.