PUBLICATION
Exposure to acrylamide disrupts cardiomyocyte interactions during ventricular morphogenesis in zebrafish embryos
- Authors
- Huang, M., Zhu, F., Jiao, J., Wang, J., Zhang, Y.
- ID
- ZDB-PUB-190113-2
- Date
- 2019
- Source
- The Science of the total environment 656: 1337-1345 (Journal)
- Registered Authors
- Keywords
- Acrylamide, Cardiac developmental toxicity, Cardiogenesis, Ventricular morphogenesis, Zebrafish embryos
- MeSH Terms
-
- Acrylamide/adverse effects*
- Animals
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/embryology
- Embryonic Development/drug effects*
- Environmental Pollutants/adverse effects*
- Morphogenesis/drug effects*
- Myocytes, Cardiac/drug effects*
- Signal Transduction/drug effects
- Zebrafish/embryology*
- PubMed
- 30625662 Full text @ Sci. Total Environ.
Citation
Huang, M., Zhu, F., Jiao, J., Wang, J., Zhang, Y. (2019) Exposure to acrylamide disrupts cardiomyocyte interactions during ventricular morphogenesis in zebrafish embryos. The Science of the total environment. 656:1337-1345.
Abstract
Acrylamide (AA), a ubiquitous chemical that is present in surrounding environment and baked or fried carbohydrate-rich food, has recently been linked to cardiac developmental toxicity. However, the toxicological role of AA exposure in the cardiac development remains largely unknown. Here we showed the cardiotoxicity of AA and its role in cardiomyocyte interactions in zebrafish embryos during ventricular morphogenesis. Using the embryo model of transgenic zebrafish Tg(Tp1:d2GFP;myl7:mCherry), we found AA interfered the dynamics of Notch signaling in the endocardium during early cardiogenesis. Prolonged exposure to AA thickened the chamber wall and prevented the trabeculae from extending into the lumen of ventricular chamber. As a result, AA reduced the ventricular shortening fraction and spatial dimension via excessively activating the Notch signal in myocardium during cardiac maturation. Moreover, exposure to AA inhibited the re-distribution of N‑cadherin and failed to coordinate cardiomyocyte interactions between the myocardium layers due to the lack of delaminated cardiomyocytes. Therefore, AA-treated embryos exhibited subcellular pathological states including disarrayed myofibrils and abnormal morphology of mitochondria despite normal proliferation of cardiomyocytes. In addition, we found overexpression of some cardiac-specific transcription factors, such as hand2 and nkx2.5, in hearts of AA-treated embryos compared with those in control group. Our study provided the evidence that the period of ventricular chamber morphogenesis might be a vulnerable window in zebrafish, and revealed new insights into how AA might exert cardiac developmental toxicity.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping