title: Imbalance of expression of bFGF and PK1 is associated with defective maturation and antenatal placental insufficiency.
abstract: OBJECTIVE
  Defective placental maturation is associated with restricted functional capacity and adverse perinatal fetal outcomes. The aim of the study was a comparative analysis of the role of mRNA expression of various angiogenic factors in placental maturation defects.
  
  
  METHODS
  We examined the mRNA expression patterns of prokineticin 1 (PK1), its receptors (PKRs), basic-fibroblast growth factor (bFGF), vascular endothelial growth factor (VEGF) and placental growth factor (PlGF) in tissue from third-trimester placentae that exhibited delayed or accelerated villous maturation.
  
  
  RESULTS
  The expression of PK1 and PKR2 was elevated in placental tissue exhibiting accelerated maturation and a predominant differentiation of terminal villi. The opposite was found in tissue exhibiting delayed maturation and deficiency of the terminal villi. In addition, low expression of bFGF correlated with the predominant differentiation of terminal villi, whereas the opposite was observed when terminal villi were deficient. The expression of VEGF, PIGF, and PKR1 showed no significant differences between the groups.
  
  
  CONCLUSIONS
  Defective placental maturation is associated with an imbalance of expression of bFGF and PK1. Our results demonstrate an involvement of the PK1/PKR2-signalling pathway in the regulation of the functional adequate capillarization in late pregnancy. We propose the bFGF/PK1-ratio as a monitor of placental function and a possible indicator of latent clinical problems, such as placental dysfunction leading to fetal hypoxia.
authors.affiliation: Institute of Pathology, University Medical Centre of the Johannes Gutenberg University, Mainz, Germany. Electronic address: larissa.seidmann@unimedizin-mainz.de.
authors.forename: L
authors.initials: L
authors.lastname: Seidmann
authors.forename: T
authors.initials: T
authors.lastname: Suhan
authors.forename: R
authors.initials: R
authors.lastname: Unger
authors.forename: V
authors.initials: V
authors.lastname: Gerein
authors.forename: C J
authors.initials: CJ
authors.lastname: Kirkpatrick
mesh_terms: D005260:Female; D016222:Fibroblast Growth Factor 2 / Q000378:metabolism*; D005768:Gastrointestinal Hormones / Q000378:metabolism*; D006801:Humans; D010920:Placenta / Q000473:pathology; D010922:Placenta Diseases / Q000378:metabolism* / Q000473:pathology; D000072483:Placenta Growth Factor; D011247:Pregnancy; D011257:Pregnancy Proteins / Q000378:metabolism*; D011263:Pregnancy Trimester, Third; D043562:Receptors, G-Protein-Coupled / Q000378:metabolism; D018000:Receptors, Peptide / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism*; D042662:Vascular Endothelial Growth Factor, Endocrine-Gland-Derived / Q000378:metabolism*
chemical_list: D005768:Gastrointestinal Hormones; C000608036:PGF protein, human; C467610:PROK1 protein, human; C470837:PROKR1 protein, human; C470838:PROKR2 protein, human; D011257:Pregnancy Proteins; D043562:Receptors, G-Protein-Coupled; D018000:Receptors, Peptide; C467484:VEGFA protein, human; D042461:Vascular Endothelial Growth Factor A; D042662:Vascular Endothelial Growth Factor, Endocrine-Gland-Derived; D016222:Fibroblast Growth Factor 2; D000072483:Placenta Growth Factor
keywords: Capillarization; Fetal hypoxia; Maturation defect; Placental dysfunction; Prokineticin; bFGF