Regulation of 5′-promoter activity of the rat growth hormone and growth hormone-releasing hormone receptor genes in the MtT/S and MtT/E cells

Haruo Nogami, Yoshiki Hiraoka, Kinji Inoue, Sadakazu Aiso, Setsuji Hisano

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

The MtT/E and MtT/S cells have been established from a mammotrophic pituitary tumor, and postulated to be progenitor and premature growth hormone (GH) cells, respectively. The difference in the regulation of GH and GH-releasing hormone (GHRH) receptor gene transcription in relation to the developmental stage of GH cells were examined in these two cell lines. In MtT/S cells, triiodothyronine (T3), all-trans retinoic acid (RA) and 9-cis retinoic acid (9cRA) stimulated GH promoter activity but dexamethasone (DEX) did not. On the other hand, DEX stimulated GHRH-receptor promoter alone. T3, RA and 9cRA showed little effect alone but each of them augmented the effect of DEX when used together with DEX. In MtT/E cells, DEX, RA and 9cRA showed similar effect as observed in MtT/S cells on both GH and GHRH-receptor promoter activity. However, T3 neither stimulated GH promoter activity nor augmented the DEX-induced GHRH-receptor gene transcription in MtT/E cells. RT-PCR analyses revealed that both cell types expressed TRα1, TRβ1 and TRα2, but expression of TRβ2, a pituitary specific isoform of TR, was only detected in MtT/S cells. However, the deficiency of TRβ2 for its own sake does not appear to be a reason why T3 action was not observed in MtT/E cells, because co-transfection of expression plasmids for TRβ2 and RXRα failed in conferring on the cells an ability to respond to T3 by increased GH or GHRH-receptor promoter activity. These results suggest that the acquisition of mechanisms responsible for the regulation of GH or GHRH-receptor transcription by T3 may be involved in the process of functional development of GH cells.

Original languageEnglish
Pages (from-to)31-41
Number of pages11
JournalNeuroendocrinology
Volume84
Issue number1
DOIs
Publication statusPublished - 2006 Dec 1
Externally publishedYes

Keywords

  • Growth hormone
  • Growth hormone-releasing hormone receptor
  • MtT/E cells
  • MtT/S cells
  • Retinoic acid
  • Thyroid hormone
  • Thyroid hormone receptors

ASJC Scopus subject areas

  • Endocrinology
  • Neuroscience(all)

Cite this

Regulation of 5′-promoter activity of the rat growth hormone and growth hormone-releasing hormone receptor genes in the MtT/S and MtT/E cells. / Nogami, Haruo; Hiraoka, Yoshiki; Inoue, Kinji; Aiso, Sadakazu; Hisano, Setsuji.

In: Neuroendocrinology, Vol. 84, No. 1, 01.12.2006, p. 31-41.

Research output: Contribution to journalArticle

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abstract = "The MtT/E and MtT/S cells have been established from a mammotrophic pituitary tumor, and postulated to be progenitor and premature growth hormone (GH) cells, respectively. The difference in the regulation of GH and GH-releasing hormone (GHRH) receptor gene transcription in relation to the developmental stage of GH cells were examined in these two cell lines. In MtT/S cells, triiodothyronine (T3), all-trans retinoic acid (RA) and 9-cis retinoic acid (9cRA) stimulated GH promoter activity but dexamethasone (DEX) did not. On the other hand, DEX stimulated GHRH-receptor promoter alone. T3, RA and 9cRA showed little effect alone but each of them augmented the effect of DEX when used together with DEX. In MtT/E cells, DEX, RA and 9cRA showed similar effect as observed in MtT/S cells on both GH and GHRH-receptor promoter activity. However, T3 neither stimulated GH promoter activity nor augmented the DEX-induced GHRH-receptor gene transcription in MtT/E cells. RT-PCR analyses revealed that both cell types expressed TRα1, TRβ1 and TRα2, but expression of TRβ2, a pituitary specific isoform of TR, was only detected in MtT/S cells. However, the deficiency of TRβ2 for its own sake does not appear to be a reason why T3 action was not observed in MtT/E cells, because co-transfection of expression plasmids for TRβ2 and RXRα failed in conferring on the cells an ability to respond to T3 by increased GH or GHRH-receptor promoter activity. These results suggest that the acquisition of mechanisms responsible for the regulation of GH or GHRH-receptor transcription by T3 may be involved in the process of functional development of GH cells.",
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