title: Transcriptional effects of hypoxia on fusiogenic syncytin and its receptor ASCT2 in human cytotrophoblast BeWo cells and in ex vivo perfused placental cotyledons.
abstract: OBJECTIVE
  The purpose of this study was to test the hypothesis that hypoxia down-regulates placental syncytin, which could play a role in altered placentogenesis; we investigated the influence of hypoxia on syncytin and its receptor ASCT2 gene expression in BeWo cells and in ex vivo perfused human cotyledons.
  
  
  METHODS
  BeWo cells were incubated with deferoxamine or cobalt chloride under normoxia and hypoxia. Additionally, a model of dually ex vivo perfused cotyledons was applied. Under hypoxic and cobalt chloride stimuli syncytin, ASCT2, glyceraldehyde-3-phosphate dehydrogenase (GAPDH), beta-actin, and beta(2)-microglobulin (beta(2)-MG) messenger RNAs were analyzed with the use of real-time polymerase chain reaction.
  
  
  RESULTS
  Hypoxia, deferoxamine, and cobalt chloride markedly decreased syncytin messenger RNA in BeWo cells, whereas ASCT2 messenger RNA was not altered significantly. In isolated perfused cotyledons, hypoxia also reduced syncytin (P<.05) but not ASCT2 messenger RNA.
  
  
  CONCLUSIONS
  Our data provide first evidence that syncytin gene expression is down-regulated by hypoxia, which strengthens the hypothesis that syncytin is reduced in disturbed pregnancies in the course of placental hypoxia.
authors.affiliation: Department of Pediatrics, University of Erlangen-Nuremberg, Erlangen, Germany. ina.knerr@kinder.imed.uni-erlangen.de
authors.forename: Ina
authors.initials: I
authors.lastname: Knerr
authors.forename: Corina
authors.initials: C
authors.lastname: Weigel
authors.forename: Knud
authors.initials: K
authors.lastname: Linnemann
authors.forename: Jörg
authors.initials: J
authors.lastname: Dötsch
authors.forename: Udo
authors.initials: U
authors.lastname: Meissner
authors.forename: Christoph
authors.initials: C
authors.lastname: Fusch
authors.forename: Wolfgang
authors.initials: W
authors.lastname: Rascher
mesh_terms: D026962:Amino Acid Transport System ASC / Q000235:genetics*; D002460:Cell Line; D003035:Cobalt / Q000494:pharmacology; D003199:Computer Systems; D003676:Deferoxamine / Q000494:pharmacology; D015536:Down-Regulation; D005260:Female; D015686:Gene Products, env / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D000860:Hypoxia / Q000235:genetics*; D066298:In Vitro Techniques; D007502:Iron Chelating Agents / Q000494:pharmacology; D015778:Minor Histocompatibility Antigens; D010920:Placenta / Q000378:metabolism*; D016133:Polymerase Chain Reaction; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000235:genetics* / Q000378:metabolism; D012333:RNA, Messenger / Q000378:metabolism; D014158:Transcription, Genetic; D014327:Trophoblasts / Q000378:metabolism*
chemical_list: D026962:Amino Acid Transport System ASC; D015686:Gene Products, env; D007502:Iron Chelating Agents; D015778:Minor Histocompatibility Antigens; D011257:Pregnancy Proteins; D012333:RNA, Messenger; C420506:SLC1A5 protein, human; C405335:syncytin; D003035:Cobalt; C018021:cobaltous chloride; D003676:Deferoxamine