title: Expression of the nonclassic histocompatibility antigen HLA-G by preeclamptic placenta.
abstract: OBJECTIVE
  Expression of the histocompatibility antigen HLA-G may be required for appropriate invasion and remodeling of uterine spiral arteries. Inappropriate expression of this antigen may result in failure of invasion, leading to partial placental ischemia and gestational disease.
  
  
  METHODS
  To test the hypothesis that the level of expression of HLA-G is reduced in trophoblasts from patients with gestational complications (preeclampsia, intrauterine growth retardation, or gestational hypertension) compared with patients with normal pregnancy, total ribonucleic acid was isolated from the fetal membrane or decidual interface of term placenta from several patient groups. Ribonuclease protection assay was used to determine levels of HLA-G expression, which was normalized for total ribonucleic acid input with beta-actin and for trophoblast content in the tissue by cytokeratin 8.
  
  
  RESULTS
  When normalized for total ribonucleic acid input (beta-actin), term placental expression of HLA-G was reduced for all forms of preeclampsia but not for intrauterine growth retardation or gestational hypertension. When tissue expression of cytokeratin, an indicator of trophoblast input, was normalized for trophoblast input, was normalized for total ribonucleic acid input, primary preeclampsia and intrauterine growth retardation had reduced numbers of trophoblast per unit tissue. When controlled for trophoblast input HLA-G expression was similar to normal for all clinical groups, except for intrauterine growth retardation, which was slightly increased.
  
  
  CONCLUSIONS
  Level of expression of HLA-G in placental tissue was reduced in preeclampsia. This decrease in expression appears to be related to reduced numbers of trophoblasts in placental tissue examined at term from patients with primary preeclampsia.
authors.affiliation: Institute of Child Health and Human Development, California Pacific Medical Center, San Francisco 94115.
authors.forename: G T
authors.initials: GT
authors.lastname: Colbern
authors.forename: M H
authors.initials: MH
authors.lastname: Chiang
authors.forename: E K
authors.initials: EK
authors.lastname: Main
mesh_terms: D000328:Adult; D001345:Autoradiography; D016022:Case-Control Studies; D003656:Decidua / Q000276:immunology; D005260:Female; D005317:Fetal Growth Retardation / Q000276:immunology; D006680:HLA Antigens / Q000032:analysis*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000032:analysis*; D006801:Humans; D006973:Hypertension / Q000276:immunology; D010920:Placenta / Q000276:immunology*; D010929:Placentation / Q000276:immunology; D011225:Pre-Eclampsia / Q000276:immunology*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000276:immunology; D015347:RNA Probes
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I; D015347:RNA Probes