Presenter : Alice Rear
Mentor : Jeffrey Gilbert
Major : Biology and Human Physiology
Poster 37
Recent studies suggest that angiogenic dysregulation in utero impairs fetal pulmonary vascular development and arrests normal alveolarization, potentially contributing to the pathogenesis of bronchopulmonary dysplasia (BPD). Since reduced utero-placental perfusion (RUPP) induced hypertension is associated with angiogenic imbalance (soluble fms-like tyrosine kinase-1, sFlt-1; and vascular endothelial growth factor, VEGF) in the maternal circulation and amniotic fluid, we hypothesized it would result in abnormal alveolarization, diminished pulmonary vascular development, and impaired VEGF signaling in the fetal rat lung. Fetal lung tissue and amniotic fluid were collected on day 19 of gestation from RUPP and normal pregnancies (NP). A second cohort delivered pups that were weighed at birth and lungs were collected at 10 weeks of age. Fetuses from RUPP pregnancies were smaller at day 19 (2.1 vs. 2.6 g; P<0.05) of gestation and at birth (6.1 vs. 6.7 g; P<0.05) than NP offspring. Preliminary data suggests that RUPP offspring may have reduced (20% decrease) pulmonary vascularity and alveolar simplification (45% decrease in alveolar space) when compared to normal pregnant controls. VEGF receptor-2 was decreased (48%; P< 0.05) in the lungs of day 19 RUPP offspring. These data suggest that chronic placental insufficiency has detrimental effects on the developing pulmonary vasculature and alveoli, and support the hypoth- esis that angiogenic imbalance in utero may play an important role in the pathogenesis of BPD