Transcriptional regulation of the GnRH receptor gene by glucocorticoids

Mol Cell Endocrinol. 2003 Feb 28;200(1-2):89-98. doi: 10.1016/s0303-7207(02)00419-7.

Abstract

Expression of the gonadotropin-releasing hormone (GnRH) receptor gene is stimulated by dexamethasone in GnRH-deficient rodents. In this study we identify a 1226 bp sequence at the 5'-flanking region of the mouse GnRH-R gene that confers dexamethasone responsiveness when expressed in host cells. Further, a glucocorticoid antagonist blocks transcriptional activity of the mGnRHR promoter. Progressive 5'-deletion of the mGnRHR promoter localized the response sequence between the -331/-255 region. Analysis of this region revealed binding sites for the AP-1 transcription factor. Mutation in AP-1 modified the functional activity of the mGnRHR promoter following GnRH agonist or dexamethasone-stimulation. Using an electrophoretic mobility shift assay, a protein complex is shown to bind to the AP-1 site. These results suggest that AP-1 proteins and glucocorticoid receptor regulate transcription of the GnRH-R promoter in a heterologous system.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Base Sequence
  • Buserelin / agonists
  • Dexamethasone / pharmacology*
  • Gene Expression Regulation
  • Genes, jun
  • Genetic Vectors / genetics
  • Glucocorticoids / pharmacology*
  • Mice
  • Molecular Sequence Data
  • Plasmids / genetics
  • Point Mutation
  • Promoter Regions, Genetic
  • Receptors, LHRH / genetics*
  • Sequence Deletion
  • Transcription, Genetic*

Substances

  • Glucocorticoids
  • Receptors, LHRH
  • Dexamethasone
  • Buserelin