Regulation of pulmonary surfactant protein synthesis in fetal lung: a major role of glucocorticoids and cyclic AMP.

Augmented synthesis of the lipoprotein, pulmonary surfactant, is initiated in fetal lung toward the end of-gestation. Inadequate surfactant synthesis by the lungs of premature infants can result in respiratory distress syndrome, the leading cause of neonatal morbidity and mortality in developed countries. The surfactant-associated proteins act with surfactant glycerophospholipids to reduce alveolar surface tension, and mediate the reutilization of secreted surfactant components by type II cells. Genes encoding the surfactant proteins SP-A, SP-B, and SP-C have been isolated and characterized. Recent findings suggest that surfactant protein gene expression in fetal lung is under multifactortal control and is regulated by glucocorticoids, cAMP, growth factors, and insulin.