Abstract
Bronchopulmonary dysplasia (BPD), the chronic lung disease of prematurity, is associated with impaired vascular and alveolar growth. Antenatal factors contribute to the risk for developing BPD by unclear mechanisms. Endothelial progenitor cells (EPCs), such as angiogenic circulating progenitor cells (CPCs) and late-outgrowth endothelial colony-forming cells (ECFCs), may contribute to angiogenesis in the developing lung. We hypothesize that cord blood angiogenic CPCs and ECFCs are decreased in preterm infants with moderate and severe BPD.
We quantified ECFCs and the CPC-to-nonangiogenic-CPC ratio (CPC:non-CPC) in cord blood samples from 62 preterm infants and assessed their relationships to maternal and perinatal risk factors as well as BPD severity. The CPC:non-CPC ratio and ECFC number were compared between preterm infants with mild or no BPD and those with moderate or severe BPD.
ECFC number (p < 0.001) and CPC:non-CPC ratio (p < 0.05) were significantly decreased in cord blood samples of preterm infants who subsequently developed moderate or severe BPD. Gestational age and birth weight were not associated with either angiogenic marker.
Circulating vascular progenitor cells are decreased in the cord blood of preterm infants who develop moderate and severe BPD. These findings suggest that prenatal factors contribute to late respiratory outcomes in preterm infants.
- ERS
