Bronchopulmonary dysplasia (BPD) affects 20-25% of very low birthweight infants and leads to significant long-term morbidity. BPD results in part from multiple inflammatory and oxidant insults encountered in the perinatal period. Exposure to hyperoxia is thought to contribute to the pathogenesis of BPD. The major focus of our research is to further define how the neonatal lung responds to toxic exposures of oxygen. Over 100 genes orchestrating the cellular response to these insults are regulated by the transcription factor NF-?B. Clinical studies have correlated NF-?B activation in the preterm lung to an increased risk of developing BPD. Our lab is working to define how NF-?B activation modulates hyperoxic injury in the newborn lung.
In quiescent cells, NF-?B remains sequestered in the cytoplasm bound to members of the I?B family of inhibitory proteins. Following inflammatory or oxidant stress, I?B phosphorylation and degradation allow NF-?B nuclear translocation, DNA binding and either activation or repression of gene expression. By further defining the unique characteristics of I?Ba and their role in modulating hyperoxia-induced NF-?B activation, we hope to identify interventions that protect preterm infants from BPD.
- Assistant Professor of Pediatrics at University of Pennsylvania School of Medicine (2010 – 2011)
- MD, Medicine, The Johns Hoplins University School of Medicine (2001)
- BA, History, Davidson College (1997)