Role of vitamin A in lung development

There is good rationale for presuming a role for vitamin A in lung development. In situ studies have demonstrated that certain retinoic acid (RA) receptor proteins are localized in a specific fashion during fetal lung branching and airway growth. Vitamin A stores are high in fetal lung and decrease toward term, possibly being utilized for changes in lung morphogenic remodeling. The binding activity, levels and expression of the cytosolic and nuclear receptor proteins for vitamin A undergo changes before and after birth in rat lung. RA slows fetal Type II cell proliferation in culture but stimulates choline incorporation into phosphatidylcholine. RA can regulate several other factors involved in lung development such as homeobox genes, matrix molecules and certain growth factors. Further study is needed on this potential functional role of RA in lung. Retinol deficiency results in lung histopathology that is similar to bronchopulmonary dysplasia, which occurs frequently in human premature neonates. Clinical trials are attempting to define the role of supplementation of vitamin A in the prevention and treatment of that condition.