Impaired pulmonary vascular development in bronchopulmonary dysplasia

Abstract

Bronchopulmonary dysplasia (BPD), the chronic lung disease associated with preterm birth, results from the disruption of normal pulmonary vascular and alveolar growth. Though BPD was once described as primarily due to postnatal injury from mechanical ventilation and oxygen therapy after preterm birth, it is increasingly appreciated that BPD results from antenatal and perinatal factors that interrupt lung development in infants born at the extremes of prematurity. The lung in BPD consists of a simplified parenchymal architecture that limits gas exchange and leads to increased cardiopulmonary morbidity and mortality. This review outlines recent advances in the understanding of pulmonary vascular development and describes how the disruption of these mechanisms results in BPD. We point to future therapies that may augment postnatal vascular growth to prevent and treat this severe chronic lung disease.

Figure 1. Paracrine mechanisms mediate the proangiogenic effects of ECFCs and MSCs

Conditioned media (CM) is collected after 24 hours in culture with either cord blood-derived ECFCs (A) or cord blood-/marrow-derived MSCs (B). ECFC-CM and MSC-CM as well as the cells themselves promote angiogenesis both in vitro and in experimental BPD. PAEC – pulmonary artery endothelial cell; AT2 – alveolar epithelial type 2 cell; RVH – right ventricular hypertrophy; LPS – lipopolysaccharide; RLMVEC – rat lung microvascular endothelial cells