Increased apoptosis and expression of p21 and p53 in premature infant baboon model of bronchopulmonary dysplasia.

Bronchopulmonary dysplasia (BPD) is a major complication of premature infants who receive prolonged ventilatory support. The pathophysiology of BPD involves oxidant injury, baro/volutrauma, and disordered lung repair. Exposure of premature lung that is poorly adapted for air breathing (>3% oxygen in fetal lung) to a higher concentration of oxygen can cause significant oxidant injury. Cell growth and differentiation of the developing lung require selective and ordered cell division. As hyperoxia can increase the expression of cell-cycle checkpoints that can cause growth arrest of lung cells, in this report we examined the expression of checkpoint proteins p53 and p21 in a premature infant the baboon model of BPD. Additionally, we also determined whether enhanced apoptosis occurs in baboon BPD model. We have shown that p53 and p21 expression are increased in 125-day as well as 140-day premature baboons with BPD. We also demonstrate increased apoptosis in lung tissue of premature baboons with BPD. These results demonstrate that cell growth inhibition is a likely factor in the evolution of BPD. Additionally, lung cells may undergo increased apoptosis that can impair the repair process in the postventilatory recovery period.