Glucocorticoid regulation of DNA, protein and surfactant phospholipid in developing lung. Temporal relationship between growth and differentiation.
In contrast to the physiologic effects of glucocorticoids on lung saturated phosphatidylcholine (SPC) production, glucocorticoids have also been shown to inhibit fetal lung growth. We have found that at the time of increasing SPC production by the fetal rabbit, rat and chick lung there is a spontaneous fall in the DNA/protein ratio of the lung tissue, suggesting decreased cell proliferation similar to that which is seen with exogenous glucocorticoid treatment. Treatment of chick embryos with glucocorticoid causes a fall in the DNA/protein ratio and a rise in the SPC content of the lung; the antiglucocorticoid 11-deoxycortisol blocks both the spontaneous fall in the DNA/protein ratio and the rise in the lung SPC content. We conclude that there is a natural slowing of lung growth in response to endogenous glucocorticoid.
D000818:Animals; D002454:Cell Differentiation; D002645:Chickens; D003350:Cortodoxone / Q000494:pharmacology; D004247:DNA / Q000096:biosynthesis*; D003907:Dexamethasone / Q000494:pharmacology; D005260:Female; D005938:Glucocorticoids / Q000502:physiology*; D066298:In Vitro Techniques; D008168:Lung / Q000254:growth & development / Q000378:metabolism*; D009929:Organ Size / Q000187:drug effects; D011247:Pregnancy; D014176:Protein Biosynthesis; D011663:Pulmonary Surfactants / Q000096:biosynthesis*; D011817:Rabbits; D051381:Rats; D011919:Rats, Inbred Strains; D013997:Time Factors
D005938:Glucocorticoids; D011663:Pulmonary Surfactants; D003907:Dexamethasone; D004247:DNA; D003350:Cortodoxone