PUBLICATION

Bisphenol S induces ectopic angiogenesis in embryos via VEGFR2 signaling, leading to lipid deposition in blood vessels of larval zebrafish

Authors
Wang, W., Ru, S., Wang, L., Qin, J., Ru, Y., Zhang, J., Zhang, X.
ID
ZDB-PUB-200430-12
Date
2020
Source
Environmental science & technology   54(11): 6822-6831 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Larva
  • Lipids
  • Phenols
  • Sulfones*
  • Zebrafish*
PubMed
32348130 Full text @ Env. Sci. Tech.
Abstract
Bisphenol S (BPS), used as a bisphenol A substitute, has been detected in various environments. However, the safety of BPS is still unclear. Here, zebrafish embryos were exposed to BPS (0, 1, 10 and 100 μg/L) for 24 hours (h), 48 h, 72 h, 96 h, and 15 days. BPS induced ectopic sprouting of budding blood vessels in embryos, but the blood flow velocity within these lesions was unchanged at 48 h. At 72 h postfertilization (hpf), by observing the subintestinal venous plexus responsible for yolk absorption, we found that VEGFR2 transduced an angiogenic signal and that the subsequent reduction in blood flow velocity inhibited yolk absorption. At 96 hpf, yolk consumption was still delayed due to the disturbed transportation route, resulting in transient extensive lipid retention in the blood vessels. After feeding, obvious atherogenic lipids were discovered in the blood vessels, especially in bends, bifurcations, and stenoses. This dynamic visualization of the pathogenesis demonstrates a plausible mechanistic link between BPS exposure-induced embryonic vessel overgrowth and an increased atherosclerosis risk.
Genes / Markers
Figures
Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping