PUBLICATION
Malachite green induces cardiovascular defects in developing zebrafish (Danio rerio) embryos by blocking VEGFR-2 signaling
- Authors
- Jang, G.H., Park, I.S., Lee, S.H., Huh, T.L., and Lee, Y.M.
- ID
- ZDB-PUB-090417-3
- Date
- 2009
- Source
- Biochemical and Biophysical Research Communications 382(3): 486-491 (Journal)
- Registered Authors
- Huh, Tae-Lin
- Keywords
- Malachite green, Cardiovascular defect, Zebrafish, VEGFR2 phosphorylation, Toxicity
- MeSH Terms
-
- Animals
- Apoptosis
- Bradycardia/chemically induced
- Cardiovascular Abnormalities/chemically induced*
- Cardiovascular Abnormalities/enzymology
- Cells, Cultured
- Coloring Agents/toxicity*
- Embryo, Nonmammalian/abnormalities
- Embryo, Nonmammalian/drug effects
- Embryo, Nonmammalian/enzymology
- Endothelium, Vascular/abnormalities
- Endothelium, Vascular/drug effects
- Endothelium, Vascular/enzymology
- Fungicides, Industrial/toxicity*
- Hematopoiesis/drug effects
- Humans
- Neovascularization, Physiologic
- Phosphorylation/drug effects
- Rosaniline Dyes/toxicity*
- Vascular Endothelial Growth Factor Receptor-2/antagonists & inhibitors*
- Vascular Endothelial Growth Factor Receptor-2/metabolism
- Zebrafish/abnormalities*
- PubMed
- 19364469 Full text @ Biochem. Biophys. Res. Commun.
Citation
Jang, G.H., Park, I.S., Lee, S.H., Huh, T.L., and Lee, Y.M. (2009) Malachite green induces cardiovascular defects in developing zebrafish (Danio rerio) embryos by blocking VEGFR-2 signaling. Biochemical and Biophysical Research Communications. 382(3):486-491.
Abstract
Malachite green (MG) is a triphenyl methane dye used in various fields that demonstrates high toxicity to bacteria and mammalian cells. When bud stage zebrafish embryos were treated with MG at 125, 150, and 175ppb for 14h, the development of trunk including intersomitic vessels was inhibited in MG-treated flk-1-GFP transgenic embyos. MG clearly induced whole growth retardation. MG induced severe cell death in trunk intersomite region of zebrafish embryos and in human vascular endothelial cells in a dose-dependent manner. MG inhibited heart rates and cardiac looping. MG attenuated whole blood formation and inhibited vascular endothelial growth factor (VEGF)-induced receptor (R)-2 phosphorylation in vascular endothelial cells. In conclusion, MG significantly alters the cardiovascular development causing growth retardation in zebrafish through the blocking VEGFR-2 activation in early cardiovascular development. It suggests that MG may be an environmental toxic agent with the potential to induce embryonic cardiovascular defects in vertebrates.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping