Glucocorticoid inhibition of RNA synthesis responsible for cleft palate in mice: a model.
A study was undertaken to elucidate the molecular mechanisms by which glucocorticoids induce cleft palate in mice. It was hypothesized that a compound such as triamcinolone acetonide inhibits mRNA synthesis; that this results later in depressed protein synthesis; and that the latter is ultimately responsible for slowed palate formation and cleft palate. Support for the model derives from the fact that the palatine shelves rise and fuse 3-4 days after the most sensitive time of administration of steroid; RNA synthesis was markedly inhibited 6-24 hr after its administration; and coadministration of cycloheximide partially reversed the tendency toward cleft palate formation.
D000818:Animals; D002247:Carbon Isotopes; D002972:Cleft Palate / Q000139:chemically induced*; D003513:Cycloheximide / Q000494:pharmacology; D003864:Depression, Chemical; D005260:Female; D005865:Gestational Age; D007930:Leucine / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D008954:Models, Biological; D009963:Orotic Acid / Q000378:metabolism; D011247:Pregnancy; D014176:Protein Biosynthesis; D012313:RNA / Q000096:biosynthesis*; D012333:RNA, Messenger / Q000096:biosynthesis; D013997:Time Factors; D014221:Triamcinolone; D014222:Triamcinolone Acetonide / Q000494:pharmacology; D014316:Tritium
D002247:Carbon Isotopes; D012333:RNA, Messenger; D014316:Tritium; D014221:Triamcinolone; D009963:Orotic Acid; D012313:RNA; D003513:Cycloheximide; D014222:Triamcinolone Acetonide; D007930:Leucine