翌圣生物 Yeasen｜生命科学试剂与诊断原料一站式平台

Abstract

Microvessels are frequently damaged, yet the in vivo temporal logic that couples endothelial gap closure to barrier resealing, and the immune-cell interactions that coordinate these steps, remains poorly defined. Using live imaging of laser-injured zebrafish intersegmental vessels, we define a staged repair program: endothelial cells migrate to bridge the gap, trapped erythrocytes are cleared, and vascular permeability rises transiently before resealing. Neutrophils arrive first, whereas macrophages persist and undergo a neutrophil-dependent functional transition. Early tnfa -associated macrophages promote endothelial migration and erythrocyte debris removal, while later ccl34a . 4 + pro-remodeling macrophages support barrier restoration. Neutrophil ablation delays this transition and selectively prolongs permeability defects. Neutrophils release CD63 + extracellular vesicles that are taken up by macrophages, and inhibiting EV/exosome secretion phenocopies key features of neutrophil loss. These findings provide a temporal framework to dissect immune-endothelial coordination during microvascular repair.