# Angiogenesis Suppression via VEGF–VEGFR2 Inhibition and Stromal–Endothelial Crosstalk Disruption by Myrosinase-Activated Broccoli Extract

## TL;DR

This study shows that myrosinase-activated broccoli extract can suppress blood vessel growth by targeting key signaling pathways in endothelial and fibroblast cells.

## Contribution

The study is the first to explore how myrosinase-activated broccoli extract affects angiogenesis and stromal-endothelial interactions.

## Key findings

- MaBE inhibited endothelial cell viability, migration, and tube formation in a dose-dependent manner.
- MaBE suppressed fibroblast-driven endothelial migration and capillary-like structure formation.
- MaBE disrupted VEGF and angiogenin signaling in fibroblasts, affecting endothelial behavior.

## Abstract

Dysregulated angiogenesis is involved in cancer and numerous ischemic, autoimmune and inflammatory diseases, prompting extensive research that has yielded a growing array of angiogenesis-modulating molecules used in clinical practice. The dietary phytocomplex of Cruciferous vegetables exhibits multiple biological activities in both in vitro and in vivo models. However, the impact of a myrosinase-activated broccoli extract (MaBE) on angiogenesis, as well as on stromal–endothelial interactions governing endothelial cell behavior, has not yet been explored. We investigated the effects of MaBE on endothelial–stromal crosstalk using endothelial cells (HUVECs) and fibroblasts (HFF1) both individually and in a fibroblast-conditioned medium model. MaBE dose-dependently inhibited endothelial viability, migration and tube formation, key steps of angiogenesis, through interference with the VEGF–VEGFR2 axis. Notably, MaBE also markedly suppressed HFF1-driven HUVEC migration and capillary-like structure formation, likely through the inhibition of fibroblast motility and the downregulation of VEGF and angiogenin signaling in HFF1 cells. Overall, these findings provide new insight into MaBE regulation of pro-angiogenic behaviors in both endothelial cells and fibroblasts while disrupting their functional interplay. By targeting multiple cellular compartments and key mediators involved in angiogenesis, MaBE emerges as a promising bioactive extract with potential relevance for the management of pathological angiogenesis-related disorders.