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Microcystin-LR induces angiodysplasia and vascular dysfunction through promoting cell apoptosis by the mitochondrial signaling pathway.
- Source :
-
Chemosphere . Mar2019, Vol. 218, p438-448. 11p. - Publication Year :
- 2019
-
Abstract
- Abstract The harmful algal blooms are becoming increasingly problematic in the regions that drinking water production depends on surface waters. With a global occurrence, microcystins are toxic peptides produced by multiple cyanobacterial genera in the harmful algal blooms. In this study, we examined the effects of microcystin-LR (MC-LR), a representative toxin of the microcystin family, on vascular development in zebrafish and the apoptosis of human umbilical vein endothelial cells (HUVECs). In zebrafish larvae, MC-LR induced angiodysplasia, damaged vascular structures and reduced lumen size at 0.1 μM and 1 μM, leading to the decrease of the blood flow area in the blood vessels and brain hemorrhage, which showed that MC-LR could dose-dependently inhibit vascular development and cause vascular dysfunction. In MC-LR treated HUVECs, the proportion of early apoptosis and late apoptosis cells increased in a concentration-dependent manner. Different concentrations of MC-LR could also activate caspase 3/9 in HUVECs, increase the level of mitochondrial ROS and reduce mitochondrial membrane potential. Additionally, MC-LR could promote the expression of p53 and inhibit the expression of PCNA. The findings showed that MC-LR could promote apoptosis of HUVECs through the mitochondrial signaling pathway. Combined with these results, MC-LR may promote vascular endothelial cell apoptosis through mitochondrial signaling pathway, leading to angiodysplasia and vascular dysfunction. Graphical abstract Image 1 Highlights • Microcystin-LR induces angiodysplasia and vascular dysfunction. • Microcystin-LR damages vascular structures and reduces lumen size. • Microcystin-LR reduces vascular patency. • Microcystin-LR causes brain hemorrhage. • Microcystin-LR promotes cell apoptosis by the mitochondrial signaling pathway. [ABSTRACT FROM AUTHOR]
Details
- Language :
- English
- ISSN :
- 00456535
- Volume :
- 218
- Database :
- Academic Search Index
- Journal :
- Chemosphere
- Publication Type :
- Academic Journal
- Accession number :
- 133781488
- Full Text :
- https://doi.org/10.1016/j.chemosphere.2018.11.019