Role of Caveolin-1 in Hyperoxia-Induced Lung Injury and Bronchopulmonary Dysplasia in Neonatal Mice
Session Number
3
Advisor(s)
Richard Minshall, UIC
Location
A147
Discipline
Medical and Health Sciences
Start Date
15-4-2026 2:15 PM
End Date
15-4-2026 3:00 PM
Abstract
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects preterm infants. It is recognized as a disorder of disrupted lung development that stems from an imbalance between lung injury and repair in immature lungs exposed to factors such as hyperoxia, mechanical ventilation, inflammation, and infection. This disruption interferes with alveolar and pulmonary vascular growth and causes impaired distal lung epithelial differentiation, resulting in structural abnormalities that increase the risk of pulmonary hypertension and long-term pulmonary morbidity. This project aims to determine whether reduced expression of the protein Caveolin-1 (Cav-1) in endothelial and epithelial cells of the lung contributes to BPD-like pathology. Thus, I plan to investigate whether Cav-1 deficiency in the context of hyperoxia is associated with defects in epithelial barrier stability or cell maturation during hyperoxia-induced BPD
Role of Caveolin-1 in Hyperoxia-Induced Lung Injury and Bronchopulmonary Dysplasia in Neonatal Mice
A147
Bronchopulmonary dysplasia (BPD) is a chronic lung disease that primarily affects preterm infants. It is recognized as a disorder of disrupted lung development that stems from an imbalance between lung injury and repair in immature lungs exposed to factors such as hyperoxia, mechanical ventilation, inflammation, and infection. This disruption interferes with alveolar and pulmonary vascular growth and causes impaired distal lung epithelial differentiation, resulting in structural abnormalities that increase the risk of pulmonary hypertension and long-term pulmonary morbidity. This project aims to determine whether reduced expression of the protein Caveolin-1 (Cav-1) in endothelial and epithelial cells of the lung contributes to BPD-like pathology. Thus, I plan to investigate whether Cav-1 deficiency in the context of hyperoxia is associated with defects in epithelial barrier stability or cell maturation during hyperoxia-induced BPD