title: Angiogenic dysfunction in molar pregnancy.
abstract: OBJECTIVE
  Molar pregnancy is associated with very early-onset preeclampsia. Since excessive circulating antiangiogenic factors may play a pathogenic role in preeclampsia, we hypothesized that molar placentas produce more antiangiogenic proteins than normal placentas.
  
  
  METHODS
  This retrospective case-control study used a semiquantitative immunohistochemical technique to compare histologic sections of molar placentas to normal controls. Tissue slides were treated with 2 antisera: one recognized the antiangiogenic markers fms-like tyrosine kinase receptor 1 (Flt1) and its soluble form (sFlt1), while the other recognized vascular endothelial marker CD31. Stain intensity was graded from 1+ (strong focal staining) to 4+ (91-100% staining).
  
  
  RESULTS
  Molar placentas (n = 19) showed significantly more staining than controls (n = 16) for Flt/sFlt1 (P < .0001).
  
  
  CONCLUSIONS
  There was a significant difference in Flt1/sFlt1 immunostaining intensity when molar placentas were compared to controls. This supports a hypothesis that the phenotype of preeclampsia in molar pregnancy may result from trophoblasts overproducing at least 1 antiangiogenic protein.
authors.affiliation: Department of Obstetrics and Gynecology, The Pritzker School of Medicine, University of Chicago, Chicago, IL, USA.
authors.forename: David
authors.initials: D
authors.lastname: Kanter
authors.forename: Marshall D
authors.initials: MD
authors.lastname: Lindheimer
authors.forename: Eileen
authors.initials: E
authors.lastname: Wang
authors.forename: Romana G
authors.initials: RG
authors.lastname: Borromeo
authors.forename: Elizabeth
authors.initials: E
authors.lastname: Bousfield
authors.forename: S Ananth
authors.initials: SA
authors.lastname: Karumanchi
authors.forename: Isaac E
authors.initials: IE
authors.lastname: Stillman
mesh_terms: D016022:Case-Control Studies; D005260:Female; D006801:Humans; D006828:Hydatidiform Mole / Q000503:physiopathology*; D007150:Immunohistochemistry; D018919:Neovascularization, Physiologic; D019408:Platelet Endothelial Cell Adhesion Molecule-1 / Q000032:analysis; D011247:Pregnancy; D012189:Retrospective Studies; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000032:analysis*
chemical_list: D019408:Platelet Endothelial Cell Adhesion Molecule-1; C501162:FLT1 protein, human; D040281:Vascular Endothelial Growth Factor Receptor-1