EXPRESSION AND MODULATION OF AQUAPORIN 5 IN HYPEROXIA-INDUCED LUNG INJURY

INTRODUCTION: Bronchopulmonary dysplasia (BPD) is a common disease that is caused by mechanical ventilation with persistent high-concentration oxygen in newborns, especially in preterm infants. One of the most important reasons is oxygen toxicosis. In physiologic conditions, liquid in the lung tissue is also transferred by aquaporins (AQPs), but the mechanism of aquaporins in hyperoxia-induced lung injury and lung dropsy is not clear. OBJECTIVE: The objective of this study was to explore the expression and the modulation of AQP5 in hyperoxia-induced lung injury. METHODS: Lung tissue was harvested after high-concentration oxygen exposure on the third, seventh, and 14th days in rats. The expression of AQP5 mRNA level and the location were detected by reverse-transcription polymerase chain reaction and immunohistochemistry, respectively, and compared with that in rats that were administered an injection of dexamethasone. RESULTS: AQP5 was strongly labeled in alveolar epithelial cells. The expression of AQP5 in hyperoxia groups (3, 7, and 14 days) revealed a notable decline as compared with the control group, with no change even in the hyperoxia 14-day group. There was no difference between hyperoxia groups and hyperoxia + dexamethasone groups on AQP5 mRNA level. CONCLUSIONS: The significant decrease of AQP5 expressed in hyperoxia-induced lung injury may be an important reason for abnormal water movement, which leads to pulmonary edema. Dexamethasone seems to have no effect in modulating AQP5 expression in acute lung injury.