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Retinoic Acids and Thyroid Hormone Act Synergistically with Dexamethasone to Increase Growth Hormone-Releasing Hormone Receptor Messenger Ribonucleic Acid Expression¹

Departments of Anatomy (H.N., K.K.) and Neurosurgery (M.K.), Keio University School of Medicine, Tokyo 160-8582; and Laboratory of Functional Anatomy, Faculty of Agriculture, Meiji University, Kanagawa 214-8571, Japan

Address all correspondence and requests for reprints to: Haruo Nogami, Ph.D., Laboratory of Neuroendocrinology, Institute of Basic Medical Sciences, University of Tsukuba, 1–1-1, Tennoudai, Tsukuba, Ibaraki 305-8575, Japan. E-mail: hnogami{at}md.tsukuba.ac.jp

The effects of all-trans-retinoic acid (RA), 9-cis-retinoic acid (9cRA), and thyroid hormone (T₃) on GH-releasing hormone receptor (GHRH-R) messenger RNA (mRNA) expression were studied using ribonuclease protection assay in the fetal rat pituitary gland and in MtT/S cells, a clonal GH cell line derived from an estrogen-induced somatotropic tumor in the rat. Although RA (1 µM), 9cRA (1 µM), or T₃ (1 nM) alone showed little effect on GHRH-R mRNA expression in the MtT/S cells, each of these substances was found to act synergistically with dexamethasone (DEX; 500 nM) to increase GHRH-R mRNA expression. The effects of RAs and T₃ were dose dependent, with maximum effects observed at 1 µM and 1 nM, respectively. The maximum effect of RAs or T₃ was not further augmented by the addition of T₃ or RAs, respectively. No apparent differences were observed in this study between the actions of RA and 9cRA. The Northern analyses showed that MtT/S cells express retinoic acid receptor 2 mRNA and thyroid hormone receptor ß2 mRNA, and DEX did not affect the levels of these mRNAs. This suggests that the role of DEX in enabling RAs or T₃ to up-regulate GHRH-R mRNA levels is not an induction of the expression of each specific receptor for RAs and T₃. The similar enhancement of DEX induction of GHRH-R mRNA by RAs or T₃ was also observed in the fetal rat pituitary gland in culture, suggesting that RA and/or T₃ is involved in the mechanisms responsible for the developmentally regulated expression of GHRH-R mRNA.

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