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Abstract
The ontogenesis of GH gene expression in the pituitary gland and immune organs of rats was studied by in vitro amplification of GH mRNA using a specific reverse transcription-polymerase chain reaction. Samples were obtained after microsurgery and total RNA extraction of fetal, neonatal and adult rat tissues. Amplification was followed by analysis using Southern blot techniques and hybridization using a specific digoxigenin-labelled GH cDNA probe. The study was started on day 15 of gestation. GH gene expression occurred in the pituitary gland on day 17. GH mRNA was found in the bone marrow and thymus of neonatal rats but not in the spleen or liver. No GH transcripts were detected in the immune organs of fetal or adult rats. The transient GH expression in rat immune organs may indicate a specific function of GH in the development of the immune system during the neonatal period.
Journal of Endocrinology (1994) 140, 137–143
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The prepro-thyrotropin-releasing hormone (ppTRH)-derived peptide, ppTRH178-199, has been proposed to inhibit ACTH release at the level of the pituitary and attenuate prolactin and behavioral responses to stress as well. The objective of this study was to elucidate a possible link between the effects of ppTRH178-199 and glucocorticoids on the inhibition of ACTH release in corticotrophs. Compared with mock-transfected cells, AtT-20 cells that were stably transfected with full-length ppTRH cDNA showed significantly increased sensitivity to dexamethasone, as measured by inhibition of ACTH release. In a group of control cells, expressing a mutated form of ppTRH cDNA lacking the ppTRH178-199 region, sensitivity to dexamethasone was not different from mock-transfected controls. Exogenous ppTRH178-199 also increased the inhibitory effect of dexamethasone in wild-type AtT-20 cells. The combined effect of dexamethasone and ppTRH cDNA in cells that express the latter was not due to increased endogenous secretion of ppTRH178-199 in response to dexamethasone, as dexamethasone was independently found to inhibit secretion of ppTRH178-199. Taken together, these data suggest that ppTRH178-199 can interact with the glucocorticoid negative feedback inhibition to regulate ACTH secretion.
