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Sex Differences in Senescence‐Related Gene Expression in a Rat Model of Bronchopulmonary Dysplasia

Bronchopulmonary dysplasia (BPD) is the most common complication of preterm birth. It is induced by hyperoxia exposure during the vulnerable saccular or early alveolar stage of lung development resulting in an arrest of alveolarization. Oxidative stress in the immature lung induced by this oxygen supplementation causes oxidative modifications leading to the initiation of senescence in damaged cells. A hallmark feature of senescence is persistent cell‐cycle arrest that is unresponsive to extrinsic or environmental growth factor induction. The senescence arrest is stringent; it is established and maintained by at least 2 major tumor suppressor pathways: the proteins p53/p21 and the p16Ink4a/retinoblastoma protein (pRb). We hypothesized that senescence is induced by hyperoxia exposure and has long term impacts in aged rats.