ABSTRACT
Surfactant-associated protein of Mr 28,000 to 35,000 (SAP-35) is an abundant glycoprotein
present in the alveolus of the lung, which imparts both structural organization to
surfactant phospholipids and provides regulatory information controlling surfactant
phospholipid secretion and metabolism. SAP-35 expression is enhanced by 3′-5′-cyclic
adenosine monophosphate and epidermal growth factor during perinatal differentiation
of type II epithelial cells. Its synthesis and RNA are also controlled by a variety
of inhibitory factors, which include transforming growth factor and insulin. Glucocorticoids
both enhance and inhibit SAP-35 expression in fetal lung explants. There is evidence
that fetal hyperinsulinemiaor hyperglycemia, or both, inhibit the morphologic differentiation
of the type II epithelial cell in association with decreased phospholipid surfactant
synthesis or secretion. Insulin is also a potent inhibitor of SAP-35 expression in
fetal lung tissue, and decreased SAP-35 was previously noted in amniotic fluid of
patients with diabetes during pregnancy. Recent progress in the management of diabetes
in pregnancy, characterized by more rigorous metabolic control, has decreased the
risk of hyaline membrane disease for the infant of the diabetic mother and is associated
with normal levels of SAP-35 in amniotic fluid. Hyaline membrane disease remains a
major cause of morbidity in infants of diabetic mothers but may also reflect a higher
incidence of premature delivery, cesarean section, and asphyxia at delivery as well
as inhibition of pulmonary surfactant phospholipid synthesis or expression of the
surfactant protein SAP-35.
