Regulation of GnRH I Receptor Gene Expression by the GnRH Agonist Triptorelin, Estradiol, and Progesterone in the Gonadotroph-Derived Cell Line αT3-1
| Autor: | J.M. Weiss, Oliver Treeck, S. Polack, Olaf Ortmann, Klaus Diedrich |
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| Rok vydání: | 2006 |
| Předmět: |
Agonist
endocrine system medicine.medical_specialty Transcription Genetic medicine.drug_class Endocrinology Diabetes and Metabolism Gonadotrophs Gonadotropic cell Cell Line Gonadotropin-Releasing Hormone Mice Endocrinology Internal medicine Gene expression medicine Animals RNA Messenger Northern blot Receptor Progesterone Triptorelin Pamoate Estradiol Chemistry Blotting Northern Triptorelin Luteolytic Agents Gene Expression Regulation Female Signal transduction Luteinizing hormone Receptors LHRH hormones hormone substitutes and hormone antagonists medicine.drug |
| Zdroj: | Endocrine. 30:139-144 |
| ISSN: | 0969-711X |
| DOI: | 10.1385/endo:30:1:139 |
| Popis: | The secretion of luteinizing hormone (LH) and the GnRH receptor (GnRH-R) concentration are modulated by ovarian steroids and GnRH. To elucidate whether this regulation is due to alterations at the transcriptional level, we examined the GnRH I-R mRNA expression in the gonadotroph-derived cell line alphaT3-1 treated with different estradiol and progesterone paradigms and the GnRH I agonist triptorelin. alphaT3-1 cells were treated with different steroid paradigms: 1 nM estradiol or 100 nM progesterone for 48 h alone or in combination. Cells were exposed to 10 nM or 100 pM triptorelin for 30 min, 3 h, 9 h, or, in pulsatile way, with a 5-min pulse per hour. The GnRH I-R mRNA was determined by Northern blot analysis. GnRH I-R mRNA from cells treated with continuous triptorelin decreased in a time- and concentration-dependent manner. Pulsatile triptorelin increased GnRH I-R gene expression. Progesterone alone further enhanced this effect, whereas estradiol and its combination with progesterone diminished it. Continuous combined treatment with estradiol and progesterone lead to a significant decrease of GnRH I-R mRNA by 30% and by 35% for estradiol alone. The addition of 10 nM triptorelin for 30 min or 3 h could not influence that steroid effect. In conclusion, estradiol and progesterone exclusively decreased GnRH I-R mRNA in alphaT3-1 cells no matter whether they are treated additionally with the GnRH I agonist triptorelin. The enhanced sensitivity of gonadotrophs and GnRH I-R upregulation by estradiol is not due to increased GnRH I gene expression because GnRH I-R mRNA is downregulated by estradiol and progesterone. Other pathways of the GnRH I-R signal transduction might be involved. |
| Databáze: | OpenAIRE |
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