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.
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism