NDLI: Pulsatile and Sustained Gonadotropin-releasing Hormone (GnRH) Receptor Signaling

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Pulsatile and Sustained Gonadotropin-releasing Hormone (GnRH) Receptor Signaling

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Pulsatile and Sustained Gonadotropin-releasing Hormone (GnRH) Receptor Signaling

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Caunt, Christopher J. Armstrong, Stephen P. Tsaneva-atanasova, Krasimira Mcardle, Craig A. Fowkes, Robert C.
Description	Author Affiliation: Armstrong SP ( Laboratories for Integrative Neuroscience and Endocrinology, Department of Clinical Science at South Bristol, University of Bristol, Whitson Street, Bristol BS1 3NY.)
Abstract	Gonadotropin-releasing hormone (GnRH) acts via 7 transmembrane region receptors on gonadotrophs to stimulate synthesis and secretion of the luteinizing hormone and follicle-stimulating hormone. It is secreted in pulses, and its effects depend on pulse frequency, but decoding mechanisms are unknown. Here we have used (nuclear factor of activated T-cells 2 (NFAT2)-emerald fluorescent protein) to monitor GnRH signaling. Increasing $[Ca^{2+}]_{i}$ causes calmodulin/calcineurin-dependent nuclear NFAT translocation, a response involving proteins (calmodulins and NFATs) that decode frequency in other systems. Using live cell imaging, pulsatile GnRH caused dose- and frequency-dependent increases in nuclear NFAT2-emerald fluorescent protein, and at low frequency, translocation simply tracked GnRH exposure (albeit with slower kinetics). At high frequency (30-min intervals), failure to return to basal conditions before repeat stimulation caused integrative tracking, illustrating how the relative dynamics of up- and downstream signals can increase efficiency of GnRH action. Mathematical modeling predicted desensitization of GnRH effects on $[Ca^{2+}]_{i}$ and that desensitization would increase with dose, frequency, and receptor number, but no such desensitization was seen in HeLa and/or LβT2 cells possibly because pulsatile GnRH did not reduce receptor expression (measured by immunofluorescence). GnRH also caused dose- and frequency-dependent activation of αGSU, luteinizing hormone β, and follicle-stimulating hormone β luciferase reporters, effects that were blocked by calcineurin inhibition. Pulsatile GnRH also activated an NFAT-responsive luciferase reporter, but this response was directly related to cumulative pulse duration. This together with the lack of desensitization of translocation responses suggests that NFAT may mediate GnRH action but is not a genuine decoder of GnRH pulse frequency.
ISSN	00219258
e-ISSN	1083351X
Journal	Journal of Biological Chemistry
Issue Number	51
Volume Number	284
Language	English
Publisher	American Society for Biochemistry and Molecular Biology (United States)
Publisher Date	2009-12-18
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Biological Clocks Physiology Calcium Signaling Cell Nucleus Metabolism Models, Biological NFATC Transcription Factors Receptors, LHRH Active Transport, Cell Nucleus Drug Effects Animals Calcineurin Genetics Calmodulin Dose-Response Relationship, Drug Gene Expression Regulation Gonadotropin-Releasing Hormone HeLa Cells Mice Research Support, Non-U.S. Gov't Biochemistry Molecular Biology
Content Type	Text
Resource Type	Article
Subject	Cell Biology Biochemistry Molecular Biology

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