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. 2019 Feb 25;10:110. doi: 10.3389/fendo.2019.00110

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Copyright © 2019 Son, Ubuka and Tsutsui.

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Regulation of GnIH promoter activity by glucocorticoid and thyroid hormone. GnIH expression is regulated by glucocorticoid (GC). GnIH neurons express GC receptor (GR) and GC-response element (GRE) is present in GnIH promoter region. Stress increases GC levels, and GC acts by binding to GR. When GC-bound GR is recruited to GRE, GnIH expression is up-regulated. GnIH expression is also actively changed by concentration of thyroid hormone (TH). Although GnIH neurons express TH receptors (TRα and β) and putative TH-response elements (TREs) exist in GnIH promoter region, TRs do not directly bind to GnIH promoter. However, thyroid status highly regulates the chromatin modification of GnIH promoter. Hypothyroidism exhibits increased GnIH expression with hyperacetylation of H3 (Ac) in promoter region. On the other hand, hyperthyroidism decreases GnIH expression associated with H3K9tri-methylation (Me).