title: Placental expression of VEGF is increased in pregnancies with hydatidiform mole: possible association with developing very early onset preeclampsia.
abstract: BACKGROUND
  Hydatidiform mole is an abnormal pregnancy with over-proliferation of the placenta, which causes the dysfunction of placenta. Although more than 80% of hydatidiform moles are benign with good outcome, hydatidiform moles are associated with developing very early onset preeclampsia. However the association between hydatidiform mole and very early onset preeclampsia is unclear. Preeclampsia is associated with altered levels of angiogenic factors, like vascular endothelial growth factor (VEGF) and soluble endoglin.
  
  
  OBJECTIVE
  The aim of this study is to investigate the levels of VEGF and endoglin in hydatidiform molar placenta.
  
  
  METHODS
  21 placentas from complete hydatidiform mole, 9 placentas from partial hydatidiform mole and 18 placentas from gestation matched placenta were collected in this study.
  
  
  METHODS
  The subjects of this study are human placentas.
  
  
  METHODS
  The protein levels and mRNA levels of VEGF and endoglin were measured using immunohistochemistry, western blotting and real time PCR.
  
  
  RESULTS
  The protein levels of VEGF measured by immunohistochemistry and western blotting were significant increased, as well as mRNA levels of VEGF quantified by real time PCR in hydatidiform molar placenta in comparison to normal controls. There was no difference in the protein levels of VEGF between complete and partial hydatidiform moles. In contrast, the levels of protein and mRNA in endoglin were no difference between hydatidiform molar placenta and normal controls.
  
  
  CONCLUSIONS
  In this study our data show that hydatidiform moles produce more VEGF than normal early pregnant placenta. The increased levels of angiogenic factors VEGF in hydatidiform moles may link to the mechanism of developing very early onset preeclampsia.
authors.affiliation: Wuxi Maternity and Child Health Hospital Affiliated Nanjing Medical University, China.
authors.forename: Min
authors.initials: M
authors.lastname: Zhao
authors.forename: Yongxiang
authors.initials: Y
authors.lastname: Yin
authors.forename: Fang
authors.initials: F
authors.lastname: Guo
authors.forename: Jiajun
authors.initials: J
authors.lastname: Wang
authors.forename: Ke
authors.initials: K
authors.lastname: Wang
authors.forename: Qi
authors.initials: Q
authors.lastname: Chen
mesh_terms: D000328:Adult; D015703:Antigens, CD / Q000235:genetics / Q000378:metabolism; D016022:Case-Control Studies; D000071063:Endoglin; D005260:Female; D015972:Gene Expression Regulation, Neoplastic; D006801:Humans; D006828:Hydatidiform Mole / Q000453:epidemiology / Q000378:metabolism*; D008875:Middle Aged; D010920:Placenta / Q000378:metabolism* / Q000473:pathology; D011225:Pre-Eclampsia / Q000453:epidemiology*; D011247:Pregnancy; D011956:Receptors, Cell Surface / Q000235:genetics / Q000378:metabolism; D012307:Risk Factors; D014158:Transcription, Genetic; D014594:Uterine Neoplasms / Q000453:epidemiology / Q000378:metabolism*; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics / Q000378:metabolism*
chemical_list: D015703:Antigens, CD; C064206:ENG protein, human; D000071063:Endoglin; D011956:Receptors, Cell Surface; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A