title: Effect of Iodide on Human Choriogonadotropin, Sodium-Iodide Symporter Expression, and Iodide Uptake in BeWo Choriocarcinoma Cells.
abstract: BACKGROUND
  Active placental transport of maternal iodide by the thyroidal sodium iodide symporter (NIS) provides an essential substrate for fetal thyroid hormone synthesis. NIS is expressed in trophoblast and is regulated by human choriogonadotropin (hCG). In thyroid, iodide down-regulates expression of several genes including NIS. Placentas of iodine-deficient rats demonstrate up-regulation of NIS mRNA, suggesting a role for iodide in regulating placental NIS.
  
  
  OBJECTIVE
  The objectives were to examine effects of iodide on expression of NIS and hCG in BeWo choriocarcinoma cells. Gene expression was studied by quantitative real-time PCR. Effects on NIS protein expression were assessed by Western blotting. Functional activity of NIS was measured by (125)I uptake. Expression of hCG protein was assessed by immunoassay of secreted hormone.
  
  
  RESULTS
  Iodide inhibited NIS mRNA and membrane protein expression as well as (125)I uptake, which were paralleled by decreased betahCG mRNA expression and protein secretion. Iodide had no effects on pendrin expression. Addition of hCG increased NIS mRNA expression. This effect was partially inhibited by addition of iodide. The inhibitory effects of iodide on NIS mRNA expression were abolished by propylthiouracil and dithiothreitol.
  
  
  CONCLUSIONS
  We conclude that expression of placental NIS is modulated by maternal iodide. This may occur through modulation of hCG effects on NIS and hCG gene expression.
authors.affiliation: Department of Endocrinology, Conjoint Endocrine Laboratory, Royal Brisbane and Women's Hospital and Queensland Health Pathology Services, Brisbane, Queensland 4029, Australia.
authors.forename: Huika
authors.initials: H
authors.lastname: Li
authors.forename: Kerry
authors.initials: K
authors.lastname: Richard
authors.forename: Brett
authors.initials: B
authors.lastname: McKinnon
authors.forename: Robin H
authors.initials: RH
authors.lastname: Mortimer
mesh_terms: D013956:Antithyroid Agents / Q000494:pharmacology; D045744:Cell Line, Tumor; D002822:Choriocarcinoma; D006063:Chorionic Gonadotropin / Q000235:genetics*; D004229:Dithiothreitol / Q000494:pharmacology; D005260:Female; D015870:Gene Expression / Q000187:drug effects; D006801:Humans; D007455:Iodine / Q000493:pharmacokinetics*; D007457:Iodine Radioisotopes; D011441:Propylthiouracil / Q000494:pharmacology; D012333:RNA, Messenger / Q000378:metabolism; D027981:Symporters / Q000235:genetics*; D013961:Thyroid Gland / Q000502:physiology; D014131:Trace Elements / Q000493:pharmacokinetics*; D014327:Trophoblasts / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D014594:Uterine Neoplasms; D000099209:Sodium-Iodide Symporters
chemical_list: D013956:Antithyroid Agents; D006063:Chorionic Gonadotropin; D004229:Dithiothreitol; D007455:Iodine; D007457:Iodine Radioisotopes; D011441:Propylthiouracil; D012333:RNA, Messenger; D027981:Symporters; D014131:Trace Elements; D000099209:Sodium-Iodide Symporters