title: Endothelial progenitor cells in mothers of low-birthweight infants: a link between defective placental vascularization and increased cardiovascular risk?
abstract: BACKGROUND
  Offspring birthweight is inversely associated with future maternal cardiovascular mortality, a relationship that has yet to be fully elucidated. Endothelial progenitor cells (EPCs) are thought to play a key role in vasculogenesis, and EPC numbers reflect cardiovascular risk.
  
  
  OBJECTIVE
  Our objective was to ascertain whether EPC number or function was reduced in mothers of low-birthweight infants.
  
  
  METHODS
  This was a prospective cohort study in a general antenatal department of a university maternity hospital.
  
  
  METHODS
  Twenty-three mothers of small for gestational age (SGA) infants (birthweight < 10th centile) and 23 mothers of appropriate for gestational age (AGA) infants (birthweight ≥ 10th centile) were recruited.
  
  
  METHODS
  Maternal EPC number and function, conventional cardiovascular risk markers, and cord blood adiponectin were measured.
  
  
  RESULTS
  Median EPC count was lower (294 vs. 367, P = 0.005) and EPC migration was reduced (0.91 vs. 1.59, P < 0.001) in SGA compared with AGA infants, with no difference in EPC adhesion (0.221 vs. 0.284 fluorescence units, P = 0.257). Maternal triglyceride levels were higher in SGA than AGA infants (0.98 vs. 0.78 mmol/liter, P = 0.006), but there was no difference in cholesterol, glucose, insulin, glycosylated hemoglobin, adiponectin, or blood pressure. There was a moderate monotone (increasing) relationship between birthweight and umbilical cord blood adiponectin (r = 0.475, P = 0.005).
  
  
  CONCLUSIONS
  Giving birth to an SGA infant was associated with lower maternal EPC number and reduced migratory function. Cord blood adiponectin was significantly correlated with birthweight.
authors.affiliation: Department of Endocrinology, Royal College of Surgeons in Ireland, Connolly Hospital, Blanchardstown, Dublin 15, Ireland.
authors.forename: Thomas F J
authors.initials: TF
authors.lastname: King
authors.forename: David A
authors.initials: DA
authors.lastname: Bergin
authors.forename: Etaoin M
authors.initials: EM
authors.lastname: Kent
authors.forename: Fiona
authors.initials: F
authors.lastname: Manning
authors.forename: Emer P
authors.initials: EP
authors.lastname: Reeves
authors.forename: Patrick
authors.initials: P
authors.lastname: Dicker
authors.forename: Noel G
authors.initials: NG
authors.lastname: McElvaney
authors.forename: Seamus
authors.initials: S
authors.lastname: Sreenan
authors.forename: Fergal D
authors.initials: FD
authors.lastname: Malone
authors.forename: John H
authors.initials: JH
authors.lastname: McDermott
mesh_terms: D000328:Adult; D002318:Cardiovascular Diseases / Q000209:etiology*; D002478:Cells, Cultured; D015331:Cohort Studies; D042783:Endothelial Cells / Q000166:cytology / Q000502:physiology*; D005260:Female; D005317:Fetal Growth Retardation / Q000209:etiology / Q000503:physiopathology; D006412:Hematopoietic Stem Cells / Q000166:cytology / Q000502:physiology*; D006801:Humans; D007230:Infant, Low Birth Weight; D007231:Infant, Newborn; D007236:Infant, Small for Gestational Age / Q000502:physiology; D009035:Mothers; D009389:Neovascularization, Pathologic / Q000150:complications*; D010920:Placenta / Q000098:blood supply* / Q000473:pathology; D010922:Placenta Diseases / Q000209:etiology / Q000503:physiopathology; D011247:Pregnancy; D011297:Prenatal Exposure Delayed Effects / Q000209:etiology; D012307:Risk Factors