title: Variable effects of maternal and paternal-fetal contribution to the risk for preeclampsia combining GSTP1, eNOS, and LPL gene polymorphisms.
abstract: OBJECTIVE
  To evaluate the maternal, paternal, and fetal genotype contribution to preeclampsia. STUDY DESIGN, MATERIALS, AND METHODS: We combined the analysis of polymorphisms of the GSTP1, eNOS, and LPL genes - affecting biotransformation enzymes and endothelial function - in a cohort of 167 preeclamptic and normal control trios (mother, father, and child) comprising a total of 501 samples in the Greek population, never analyzed before by this approach.
  
  
  RESULTS
  For the frequency of the GSTP1 Ile(105)/Val(105), the eNOS Glu298Asp and the LPL-93 polymorphisms, statistically significant differences were found between the two groups. However, the transmission rates of the parental alleles to neonates studied by the transmission disequilibrium test, disclosed no increased rate of transmission to preeclampsia children for the variant alleles of Val(105) GSTP1, 298Asp eNOS, and -93G LPL.
  
  
  CONCLUSIONS
  These novel data, suggest that interaction of all three types of genotypes (mother, father and neonate), reveals no effects on the development of preeclampsia, but provide the impetus for further studies to decipher the individual contribution of each genetic parameter of preeclampsia.
authors.affiliation: First Department of Obstetrics and Gynecology, University of Athens School of Medicine, Alexandra University Hospital, Athens, Greece. kpappa@med.uoa.gr
authors.forename: Kalliopi I
authors.initials: KI
authors.lastname: Pappa
authors.forename: Maria
authors.initials: M
authors.lastname: Roubelakis
authors.forename: George
authors.initials: G
authors.lastname: Vlachos
authors.forename: Spyros
authors.initials: S
authors.lastname: Marinopoulos
authors.forename: Antonia
authors.initials: A
authors.lastname: Zissou
authors.forename: Nicholas P
authors.initials: NP
authors.lastname: Anagnou
authors.forename: Aris
authors.initials: A
authors.lastname: Antsaklis
mesh_terms: D000328:Adult; D016022:Case-Control Studies; D015331:Cohort Studies; D015987:Effect Modifier, Epidemiologic; D005219:Father-Child Relations; D005260:Female; D005333:Fetus / Q000378:metabolism / Q000502:physiology; D020022:Genetic Predisposition to Disease; D051549:Glutathione S-Transferase pi / Q000235:genetics* / Q000502:physiology; D006801:Humans; D008071:Lipoprotein Lipase / Q000235:genetics* / Q000502:physiology; D008297:Male; D033261:Maternal-Fetal Relations / Q000502:physiology*; D052250:Nitric Oxide Synthase Type III / Q000235:genetics* / Q000502:physiology; D020641:Polymorphism, Single Nucleotide / Q000502:physiology; D011225:Pre-Eclampsia / Q000453:epidemiology / Q000209:etiology / Q000235:genetics*; D011247:Pregnancy; D012307:Risk Factors; D055815:Young Adult
chemical_list: C496314:NOS3 protein, human; D052250:Nitric Oxide Synthase Type III; C496556:GSTP1 protein, human; D051549:Glutathione S-Transferase pi; C548261:LPL protein, human; D008071:Lipoprotein Lipase