PUBLICATION
Cylindrospermopsin induces abnormal vascular development through impairing cytoskeleton and promoting vascular endothelial cell apoptosis by the Rho/ROCK signaling pathway
- Authors
- Wang, L., Chen, G., Xiao, G., Han, L., Wang, Q., Hu, T.
- ID
- ZDB-PUB-200221-7
- Date
- 2020
- Source
- Environmental research 183: 109236 (Journal)
- Registered Authors
- Keywords
- Apoptosis, Cylindrospermopsin, Rho/ROCK signaling pathway, Vascular development, Zebrafish
- MeSH Terms
-
- Animals
- Apoptosis*/drug effects
- Bacterial Toxins*/toxicity
- Cytoskeleton/drug effects
- Humans
- Signal Transduction
- Umbilical Cord/cytology
- Uracil/analogs & derivatives*
- Uracil/toxicity
- PubMed
- 32062183 Full text @ Environ. Res.
Citation
Wang, L., Chen, G., Xiao, G., Han, L., Wang, Q., Hu, T. (2020) Cylindrospermopsin induces abnormal vascular development through impairing cytoskeleton and promoting vascular endothelial cell apoptosis by the Rho/ROCK signaling pathway. Environmental research. 183:109236.
Abstract
Cylindrospermopsin (CYN) is a widely distributed cyanobacterial toxin in water bodies and is considered to pose growing threats to human and environmental health. Although its potential toxicity has been reported, its effects on the vascular system are poorly understood. In this study, we examined the toxic effects of CYN on vascular development and the possible mechanism of vascular toxicity induced by CYN using zebrafish embryos and human umbilical vein endothelial cells (HUVECs). CYN exposure induced abnormal vascular development and led to an increase in the growth of common cardinal vein (CCV), in which CCV remodeling was delayed as reflected by the larger CCV area and wider ventral diameter. CYN decreased HUVECs viability, inhibited HUVECs migration, promoted HUVECs apoptosis, destroyed cytoskeleton, and increased intracellular ROS levels. Additionally, CYN could promote the expression of Bax, Bcl-2, and MLC-1 and inhibit the expression of ITGB1, Rho, ROCK, and VIM-1. Taken together, CYN may induce cytoskeleton damage and promote vascular endothelial cell apoptosis by the Rho/ROCK signaling pathway, leading to abnormal vascular development. The current results provide potential insight into the mechanism of CYN toxicity in angiocardiopathy and are beneficial for understanding the environmental risks of CYN for aquatic organisms and human health.
Genes / Markers
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Orthology
Engineered Foreign Genes
Mapping