Macrophage Extracellular Vesicle-Packaged miR-23a-3p Impairs Maintenance and Angiogenic Capacity of Human Endothelial Progenitor Cells in Neonatal Hyperoxia-Induced Lung Injury

The authors used clodronate liposomes to deplete macrophages in a mouse model of neonatal hyperoxia-induced lung injury to evaluate if endothelial progenitor cell loss in bronchopulmonary dysplasia lungs could be an effect of macrophage infiltration.