Endothelial progenitor cells in mothers of low-birthweight infants: a link between defective placental vascularization and increased cardiovascular risk?

J Clin Endocrinol Metab. 2013 Jan;98(1):E33-9. doi: 10.1210/jc.2012-2793. Epub 2012 Nov 15.

Abstract

Context: 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.

Design and setting: This was a prospective cohort study in a general antenatal department of a university maternity hospital.

Participants: 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.

Main outcome measures: 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).

Conclusion: 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.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Cardiovascular Diseases / etiology*
  • Cells, Cultured
  • Cohort Studies
  • Endothelial Cells / cytology
  • Endothelial Cells / physiology*
  • Female
  • Fetal Growth Retardation / etiology
  • Fetal Growth Retardation / physiopathology
  • Hematopoietic Stem Cells / cytology
  • Hematopoietic Stem Cells / physiology*
  • Humans
  • Infant, Low Birth Weight*
  • Infant, Newborn
  • Infant, Small for Gestational Age / physiology
  • Mothers*
  • Neovascularization, Pathologic / complications*
  • Placenta / blood supply*
  • Placenta / pathology
  • Placenta Diseases / etiology
  • Placenta Diseases / physiopathology
  • Pregnancy
  • Prenatal Exposure Delayed Effects / etiology
  • Risk Factors