# Microinjection of angiotensin II into zebrafish embryos induces transient dilation and elastin disruption of the dorsal aorta

## TL;DR

Injecting angiotensin II into zebrafish embryos causes temporary aortic widening and disrupts elastic fiber formation in adulthood.

## Contribution

Demonstrates a novel zebrafish model for studying angiotensin II's effects on vascular development and elastic fiber formation.

## Key findings

- AngII injection increased dorsal aortic diameter by 20% in zebrafish at 5 days post-fertilization.
- Elastic fiber formation was impaired in adult zebrafish after AngII exposure.
- Matrix metalloproteinase-2 expression was elevated in the dorsal aorta of AngII-injected fish.

## Abstract

The effects of angiotensin II (AngII) on blood vessel development and remodeling have been extensively investigated in mice and humans. However, its action on the vessels in the zebrafish remains largely unknown. To investigate whether AngII affects vascular morphology in vivo, we administered AngII into the endothelial‐specific transgenic reporter zebrafish (Tg[kdrl:EGFP]) at the 1‐cell stage. The average dorsal aortic diameter of five serial positions was significantly increased by 20% in AngII‐injected zebrafish compared with buffer‐injected controls at 5 days post‐fertilization. Histological studies in AngII‐injected zebrafish at 8 weeks post‐fertilization showed that elastic fiber formation was partly attenuated, with enhanced matrix metalloproteinase‐2 expression in the dorsal aorta without dilation. These results suggest that AngII induced transient aortic expansion in early larvae and may affect vascular elastic fiber formation in adult zebrafish. The use of the AngII‐injected zebrafish model is a potential tool to dissect the mechanisms of disruption of elastic vascular wall formation in the aorta.