title: Determinants of placental vascularity.
abstract: OBJECTIVE
  Vascular growth during implantation and placentation is critical for successful gestation and it is thought that vascular insufficiencies during placentation contribute to a number of obstetrical complications. However, relatively little is known regarding the regulation of angiogenesis in the placenta.
  
  
  METHODS
  We review literature concerning the potential significance of inadequate placental vascularity as a contributor to the obstetrical complications of spontaneous abortion, fetal growth restriction and preeclampsia. Gene expression assays were used to compare fluctuations of placenta growth factor (PlGF) and PlGF receptor expression in normal and preeclamptic trophoblast in vitro.
  
  
  RESULTS
  Studies have shown that common obstetrical complications manifest altered placental vascularity. Both intrinsic defects (gene knockouts) and extrinsic factors (O(2) tension, cytokines, etc) may be responsible for the defects. Some of these factors have been shown to influence trophoblast vascular endothelial growth factor (VEGF)/PlGF expression suggesting this particular family of angiogenic proteins play an important role in placental angiogenesis.
  
  
  CONCLUSIONS
  Placental vascularization reflects a complex interaction of regulatory factors. Understanding the regulation of vascular growth in the placenta will provide much needed insight into placenta-related vascular insufficiencies.
authors.affiliation: Department of Medical Microbiology and Immunology, Southern Illinois University School of Medicine, Springfield, IL 62794-9626, USA. dtorry@siumed.edu
authors.forename: Donald S
authors.initials: DS
authors.lastname: Torry
authors.forename: Monica
authors.initials: M
authors.lastname: Hinrichs
authors.forename: Ronald J
authors.initials: RJ
authors.lastname: Torry
mesh_terms: D000022:Abortion, Spontaneous / Q000235:genetics / Q000503:physiopathology; D016228:Endothelial Growth Factors / Q000235:genetics; D016326:Extracellular Matrix Proteins / Q000235:genetics; D005260:Female; D005317:Fetal Growth Retardation / Q000235:genetics / Q000503:physiopathology; D018507:Gene Expression Regulation, Developmental; D020868:Gene Silencing; D006801:Humans; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age; D009154:Mutation; D018919:Neovascularization, Physiologic / Q000235:genetics / Q000502:physiology*; D010920:Placenta / Q000098:blood supply* / Q000378:metabolism / Q000503:physiopathology; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000235:genetics / Q000503:physiopathology; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000235:genetics
chemical_list: D016228:Endothelial Growth Factors; D016326:Extracellular Matrix Proteins; C000608036:PGF protein, human; D011257:Pregnancy Proteins; D042461:Vascular Endothelial Growth Factor A; D000072483:Placenta Growth Factor