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Structural and transcriptomic response to antenatal corticosteroids in an Erk3-null mouse model of respiratory distress.

Pew BK, Harris RA, Sbrana E, Guaman MC, Shope C, Chen R, Meloche S, Aagaard K

Department of Molecular and Cell Biology, Baylor College of Medicine, Houston, TX.

Neonatal respiratory distress syndrome in preterm infants is a leading cause of neonatal death. Pulmonary insufficiency-related infant mortality rates have improved with antenatal glucocorticoid treatment and neonatal surfactant replacement. However, the mechanism of glucocorticoid-promoted fetal lung maturation is not understood fully, despite decades of clinical use. We previously have shown that genetic deletion of Erk3 in mice results in growth restriction, cyanosis, and early neonatal lethality because of pulmonary immaturity and respiratory distress. Recently, we demonstrated that the addition of postnatal surfactant administration to antenatal dexamethasone treatment resulted in enhanced survival of neonatal Erk3-null mice.

Am. J. Obstet. Gynecol. 2016;215(3):384.e1-384.e89.

Pubmed ID: 27143398

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