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Department of Anatomy (H.N., K.K.), School of Medicine, Keio University, Tokyo 160, Japan; Department of Regulation Biology (K.I.), Faculty of Science, Saitama University, Saitama 338, Japan
Address all correspondence and requests for reprints to: Haruo Nogami, Ph.D., Department of Anatomy, School of Medicine, Keio University, 35 Shinanomachi, Shinjuku-ku, Tokyo 160, Japan.
The mechanism by which glucocorticoids induce GH expression between embryonic days 18 and 19 (E1819) in the fetal rat pituitary gland was examined with an in vitro organ culture system. Twenty-four hour incubation of E18 pituitary glands in serum-free medium containing either dexamethasone (DEX, 550 nM) or corticosterone (0.55 µM) resulted in a conspicuous accumulation of GH messenger RNA (mRNA), whereas no spontaneous expression of GH mRNA was noted without glucocorticoid. Triiodothyronine (1 nM) alone weakly induced GH mRNA but increased the effect of DEX 2-fold. The GH mRNA accumulation was not observed after 5 or 10 h incubation with DEX. However, a 10-h incubation with DEX followed by 14 h chase incubation without DEX resulted in apparent induction of GH mRNA. The induction of GH mRNA by DEX was completely inhibited by puromycin.
These data, taken as a whole, suggest that the induction of GH mRNA by DEX in the fetal pituitary gland is not a direct effect of DEX on the GH gene but is mediated by a factor that is synthesized in the pituitary gland in response to DEX. Both immunoblot and RNase protection assays suggested that this factor is not pit-1, which is known to be required for GH mRNA expression.
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