Dexamethasone affects phosphatidylinositol synthesis and degradation in cultured human embryonic cells.
Dexamethasone (DEX), a glucocorticoid which induces cleft palate, causes marked alterations in the synthesis and degradation of phosphatidylinositol (PI) but not phosphatidylcholine in an established fibroblastic cell line derived from a human embryonic palate. Incorporation of radiolabeled inositol into phosphatidylinositol as well as degradation of prelabeled phosphatidylinositol is stimulated by DEX. The dose-response curves for the DEX-induced effect on PI synthesis and DEX-induced inhibition of cell proliferation are nearly identical, with the maximal responses occurring at 10(-8)M DEX. Our results suggest that DEX-induced inhibition of human embryonic palatal mesenchyme cell proliferation and alterations in synthesis and degradation of phosphatidylinositol are related.
D002455:Cell Division / Q000187:drug effects; D002460:Cell Line; D003907:Dexamethasone / Q000494:pharmacology*; D004622:Embryo, Mammalian; D005260:Female; D006801:Humans; D007700:Kinetics; D010159:Palate / Q000196:embryology; D010716:Phosphatidylinositols / Q000096:biosynthesis / Q000378:metabolism*; D011247:Pregnancy; D014316:Tritium
D010716:Phosphatidylinositols; D014316:Tritium; D003907:Dexamethasone