Phenanthrene exposure produces cardiac defects during embryo development of zebrafish (Danio rerio) through activation of MMP-9

• Main Authors: Zhang, Youyu, Huang, Lixing, Wang, Chonggang, Gao, Dongxu, Zuo, Zhenghong, 王重刚, 左正宏
• Format: Article in Journal/Newspaper
• Language: English
• Published: PERGAMON-ELSEVIER SCIENCE LTD 2013
• Subjects: POLYCYCLIC AROMATIC-HYDROCARBONS; MATRIX-METALLOPROTEINASE ACTIVITY; SALMON ONCORHYNCHUS-GORBUSCHA; HEART-FAILURE; DILATED CARDIOMYOPATHY; CRUDE-OIL; MYOCARDIAL-INFARCTION; TARGETED DELETION; GELATINASE-B; EXPRESSION; Oncorhynchus gorbuscha
• Online Access: http://dspace.xmu.edu.cn/handle/2288/90674

National Natural Science Foundation of China [20877064]; Fundamental Research Funds for the Central Universities [2012121045]; National Foundation for fostering talents of basic science [J1030626] Phenanthrene (Phe) is one of the most abundant polycyclic aromatic hydrocarbons in the aquatic environment as a result of human activities. It is widely accepted that Phe has cardiotoxic effects. Even so, knowledge concerning the mechanism(s) of cardiac development toxicity is still limited. In this study, we exposed zebrafish embryos to environmentally relevant concentrations of Phe and then investigated its cardiotoxic effects and the mechanism(s) involved. Some cardiac morphogenetic defects, which was characterized by an abnormally looped and enlarged heart, dilated and thinner ventricular wall, and increased interstitial fibrosis, were observed in the Phe treated groups. The mRNA and protein expression levels of matrix metalloproteinase-9 (MMP-9), as well as the MMP-9 activity, were induced. Moreover, during co-treatment of the zebrafish embryos with MMP-9 inhibitor, the cardiac defects caused by Phe were attenuated. In addition, Phe exposure led to an up-regulation of transforming growth factor (TGF-beta), which plays a crucial role in mediating cardiac fibrosis. Taken together, our data indicated that the exposure to Phe of zebrafish embryos disrupted normal cardiac development, and that the cardiac defects induced by Phe were mediated by the MMP-9, while TGF-beta was also involved in these cardiac defects. (C) 2013 Elsevier Ltd. All rights reserved.