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Decrease and dysfunction of endothelial progenitor cells in umbilical cord blood with maternal pre-eclampsia.

Liang Xia1, Xin P Zhou, Jun H Zhu

  • 1Department of Cardiovascular Diseases, the First Affiliated Hospital, Medical School of Zhejiang University, Hangzhou, China.

The Journal of Obstetrics and Gynaecology Research
|August 11, 2007
PubMed
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Pre-eclampsia is linked to lower numbers and impaired function of placental/fetal endothelial progenitor cells (EPCs). These alterations correlate with increased soluble fms-like tyrosine kinase 1 (sFlt-1) levels in umbilical cord blood.

Area of Science:

  • Obstetrics and Gynecology
  • Vascular Biology
  • Reproductive Medicine

Background:

  • Pre-eclampsia involves defective placental angiogenesis and maternal vascular dysfunction.
  • Reduced endothelial progenitor cells (EPCs) are observed in maternal circulation with pre-eclampsia.
  • EPCs are crucial for neovascularization and reendothelialization.

Purpose of the Study:

  • To investigate the presence of EPC depletion in placental/fetal circulation of pre-eclamptic pregnancies.
  • To assess the functional capacity of EPCs in pre-eclampsia.

Main Methods:

  • Collected venous cord blood from pre-eclamptic (n=14) and normotensive (n=10) mothers.
  • Enumerated circulating EPCs (AC133+/KDR+) using fluorescence-activated cell sorting (FACS).

Related Experiment Videos

  • Assessed in vitro EPC proliferation, migration, and vasculogenesis.
  • Main Results:

    • Significantly decreased circulating EPC numbers in pre-eclampsia group compared to controls (P < 0.001).
    • Reduced EPC numbers also observed after in vitro cultivation (P < 0.001).
    • Impaired proliferation, migration, and vasculogenesis capacities of EPCs from pre-eclamptic patients.

    Conclusions:

    • Documented decreased numbers and dysfunction of placental/fetal circulating EPCs in pre-eclampsia.
    • Alterations in EPCs are likely associated with elevated sFlt-1 levels in umbilical cord blood.