title: Maternal endothelial progenitor colony-forming units with macrophage characteristics are reduced in preeclampsia.
abstract: BACKGROUND
  Endothelial progenitor cells (EPCs) provide paracrine support to the vascular endothelium and may also replace damaged or senescent endothelial cells. Low numbers of endothelial progenitor colony-forming units (CFU-ECs) in culture are a predictive biomarker of vascular disease. We hypothesized that the number of CFU-ECs derived from maternal blood are decreased in women with preeclampsia compared to normal pregnancy.
  
  
  METHODS
  Primigravid women with singleton normal (n = 12) or preeclamptic (n = 12) pregnancies were studied during the third trimester. The culture assay was performed using a pre-plating step to eliminate mature endothelial cells and nonprogenitor cells; colonies per well were counted and further characterized.
  
  
  RESULTS
  Colony numbers were fourfold lower on average in preeclampsia compared to control samples (P < 0.005). A majority of the cells comprising individual colonies were positive for both endothelial (Ulex europaeus lectin staining and acetylated low-density lipoprotein (LDL) uptake) and monocyte/macrophage (CD45, CD14, CD115) characteristics. The SRY gene was detected in CFU-ECs derived from umbilical cord blood samples from male fetuses but not in CFU-ECs from peripheral blood of mothers with male fetuses. Maternal plasma concentrations of the antiangiogenic factor, soluble fms-like tyrosine kinase-1 (sFlt-1) were elevated (P < 0.0001) whereas placental growth factor (PlGF) was reduced (P < 0.01) in women with preeclampsia, but these factors did not correlate with CFU-EC counts.
  
  
  CONCLUSIONS
  CFU-ECs derived from culture of peripheral blood mononuclear cells, a correlate of cardiovascular risk in nonpregnancy populations, are rarified in women with preeclampsia compared to normal pregnancy. PCR analysis is consistent with a maternal origin of these cells.
authors.affiliation: Department of Obstetrics, Gynecology and Reproductive Sciences, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania, USA.
authors.forename: Carol
authors.initials: C
authors.lastname: Lin
authors.forename: Augustine
authors.initials: A
authors.lastname: Rajakumar
authors.forename: Daniel A
authors.initials: DA
authors.lastname: Plymire
authors.forename: Vivek
authors.initials: V
authors.lastname: Verma
authors.forename: Nina
authors.initials: N
authors.lastname: Markovic
authors.forename: Carl A
authors.initials: CA
authors.lastname: Hubel
mesh_terms: D000328:Adult; D042783:Endothelial Cells / Q000166:cytology*; D005260:Female; D024282:Genes, sry / Q000235:genetics; D006801:Humans; D008264:Macrophages / Q000276:immunology*; D008297:Male; D000072483:Placenta Growth Factor; D011225:Pre-Eclampsia / Q000097:blood*; D011247:Pregnancy; D011249:Pregnancy Complications, Cardiovascular / Q000276:immunology / Q000473:pathology; D011257:Pregnancy Proteins / Q000097:blood; D011263:Pregnancy Trimester, Third; D012243:Rhodopsin / Q000235:genetics; D013234:Stem Cells / Q000166:cytology* / Q000276:immunology; D040281:Vascular Endothelial Growth Factor Receptor-1 / Q000097:blood
chemical_list: C000608036:PGF protein, human; D011257:Pregnancy Proteins; D000072483:Placenta Growth Factor; D012243:Rhodopsin; D040281:Vascular Endothelial Growth Factor Receptor-1