Bronchopulmonary dysplasia (BPD) is the most common chronic lung disease in premature infants. Our research group has previously shown that placentas of infants with BPD have a lower placental villous vascularity as compared to the placentas of premature infants who do not develop BPD. Our epidemiological studies of archived placental specimens from the Prentice NICU cohort (spanning 2005 to present) consistently demonstrate that the vascular structure of the placenta closely mirrors that of neonatal lung structure and function. An important next step in our placental research is to identify promising genetic markers of placental vascular dysfunction that will enhance the prediction and understand the pathophysiology of neonatal chronic lung disease (BPD). FOXF1 is a transcription factor which regulates vasculogenesis in various organs and is highly expressed in the placenta throughout pregnancy. Our research team has also found that FOXF1 gene expression is decreased in the lungs of patients who have alveolar capillary dysplasia (ACD), a congenital lung disease associated with neonatal death due to pulmonary vascular dysfunction and severe respiratory failure. FOXF1 gene expression has not been previously studied in placentas of premature infants who go on to develop BPD, which is often thought to be a premature infant form of ACD. We hypothesize that FOXF1 gene and its protein expression are similarly down regulated in placentas of premature infants who develop BPD. We will test this hypothesis using placental specimens from infants born at Prentice Women’s Hospital.
|Effective start/end date||9/1/16 → 8/31/18|
- Northwestern Memorial Hospital (Agmt 8/24/17)
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