Hyperoxia-induced lung injury increases CDKN1A levels in a newborn rat model of bronchopulmonary dysplasia

Abstract

Bronchopulmonary dysplasia (BPD) is a common, chronic lung disease of infants. Presently, high oxygen exposure and mechanical ventilation considerably influence the development of BPD. To clarify the pathological mechanisms of this disease, we developed a hyperoxia-induced BPD rat model and investigated the role of CDKN1A in the pathogenesis of BPD. Newborn rats were randomly assigned to the hyperoxia (85% O2) and control (normoxia, 21% O2) groups. Lung tissues were collected on days 1, 3, 7, 14, or 21 after the start of hyperoxia or normoxia exposure. The expression of CDKN1A was detected by immunohistochemistry, western blot, and real-time PCR. Starting from day 3, CDKN1A mRNA expression was higher in the hyperoxia group. From day 7, the radial alveolar count was significantly different between the two groups, and on day 14, the hyperoxia group had high CDKN1A protein expression compared to the control group. These results suggest that increased CDKN1A expression may be involved in the pathogenesis of BPD through alveolarization and lung retardation.