title: Role of GnRH-GnRH receptor signaling at the maternal-fetal interface.
abstract: OBJECTIVE
  To investigate the expression and function of GnRH and GnRH receptor (GnRHR) subtypes at the maternal-fetal interface.
  
  
  METHODS
  In vitro experiments using freshly isolated human trophoblast cells, decidual stromal cells (DSCs), and immortalized cell lines.
  
  
  METHODS
  University teaching hospital.
  
  
  METHODS
  Placenta-fetal membranes from term deliveries.
  
  
  METHODS
  Human trophoblast and DSCs were isolated, purified, and cultured.
  
  
  METHODS
  Expression of GnRH-I, GnRH-II, and GnRHR-I mRNA and protein in human trophoblast cell lines and tissues were evaluated by reverse-transcription polymerase chain reaction and Western blot. The effect of GnRH-I and -II on the production of select cytokines (hCG, interleukin [IL] 8, IL-6, matrix metalloproteinase 3, monocyte chemoattractant protein 1, vascular endothelial growth factor, soluble Fms-like tyrosine kinase 1, urokinase-type plasminogen activator, and plasminogen activator inhibitor 1) were measured by ELISA and normalized for protein content.
  
  
  RESULTS
  GnRH-I, GnRH-II, and GnRHR-I mRNA and protein were identified in trophoblasts and decidua. GnRH-I and -II stimulated hCG production by trophoblast and trophoblast-derived cell lines in a dose-dependent fashion (e.g., 2.8-fold, from 2.5 ± 0.5 to 7.0 ± 0.4 ng/mg protein per 24 h, for 1,000 nmol/L GnRH-I and 2.4-fold, from 2.5 ± 0.5 to 6.1 ± 0.6 ng/mg protein per 24 h, for 1,000 nmol/L GnRH-II) without affecting the production of other cytokines.
  
  
  CONCLUSIONS
  Trophoblasts and decidua express GnRH-I, GnRH-II, and GnRHR-I mRNA and protein. GnRH-I and -II selectively stimulate hCG production by trophoblast cells without altering the production of select cytokines by trophoblasts or decidua. The role of GnRH-GnRHR signaling at the maternal-fetal interface therefore appears to be limited to the regulation of trophoblast hCG production.
authors.affiliation: Department of Obstetrics and Gynecology, Catholic University of Korea, Seoul, South Korea.
authors.forename: Hee Joong
authors.initials: HJ
authors.lastname: Lee
authors.forename: Victoria V
authors.initials: VV
authors.lastname: Snegovskikh
authors.forename: Joong Shin
authors.initials: JS
authors.lastname: Park
authors.forename: Nastaran
authors.initials: N
authors.lastname: Foyouzi
authors.forename: Ku Taek
authors.initials: KT
authors.lastname: Han
authors.forename: Eric J
authors.initials: EJ
authors.lastname: Hodgson
authors.forename: Seth
authors.initials: S
authors.lastname: Guller
authors.forename: Errol R
authors.initials: ER
authors.lastname: Norwitz
mesh_terms: D000818:Animals; D002478:Cells, Cultured; D002522:Chlorocebus aethiops; D006063:Chorionic Gonadotropin / Q000235:genetics / Q000378:metabolism; D005321:Extraembryonic Membranes / Q000378:metabolism / Q000502:physiology; D005260:Female; D007987:Gonadotropin-Releasing Hormone / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D006801:Humans; D033261:Maternal-Fetal Relations / Q000502:physiology*; D051379:Mice; D010920:Placenta / Q000378:metabolism / Q000502:physiology; D011247:Pregnancy; D011261:Pregnancy Trimester, First / Q000235:genetics / Q000378:metabolism / Q000502:physiology; D011966:Receptors, LHRH / Q000235:genetics / Q000378:metabolism / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014327:Trophoblasts / Q000378:metabolism / Q000502:physiology
chemical_list: D006063:Chorionic Gonadotropin; D011966:Receptors, LHRH; D007987:Gonadotropin-Releasing Hormone