Glucocorticoid receptor-mediated regulation of Rfrp (GnIH) and Gpr147 (GnIH-R) synthesis in immortalized hypothalamic neurons

MOLECULAR AND CELLULAR ENDOCRINOLOGY

卷:384

Article

Gojska, Nicole M.¹  Belsham, Denise D.^1,2,3,4 

[1] Univ Toronto, Dept Physiol, Toronto, ON M5S 1A8, Canada

[2] Univ Toronto, Dept Med, Toronto, ON M5S 1A8, Canada

[3] Univ Toronto, Dept Obstet & Gynaecol, Toronto, ON M5S 1A8, Canada

[4] Univ Hlth Network, Toronto Gen Hosp, Res Inst, Div Cellular & Mol Biol, Toronto, ON M5S 1A8, Canada

关键词: RFamide-related peptide;    GnIH;    GPR147;    Hypothalamus;    Stress;    Glucocorticoids;   

DOI  :  10.1016/j.mce.2013.12.015

来源: Elsevier

【 摘 要 】

A novel RFamide peptide, gonadotropin-inhibitory hormone (GnIH) has emerged as a modulator of avian reproduction. However, the functional role of the mammalian homologue, RFRP-3 remains poorly understood. The RFRP-3 neuronal circuit is influenced by the stress axis. However, whether the Rfrp gene is under direct glucocorticoid (GC)-mediated transcriptional regulation, in the presence and absence of the gonadal steroid, 17 beta-estradiol, is unknown. We investigated the regulation of the Rfrp (GnIH) and Gpr147 (GnIH-R) transcripts by steroids in a novel hypothalamic Rfrp-expressing cell model, rHypoE-23. The GC agonist, dexamethasone increased Rfrp and Gpr147 mRNA levels. Dexamethasone acted directly on the nuclear GC receptor (GR) to mediate GC-dependent transcriptional changes, independently of de novo protein synthesis. 17 beta-estradiol had no significant effect on Rfrp or Gpr147 biosynthesis in these neurons. This suggests that Rfrp-expressing neurons serve as potential upstream mediators of stress-induced effects through GR-dependent mechanisms. (C) 2013 Elsevier Ireland Ltd. All rights reserved.

【 授权许可】

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