title: Decrease and senescence of endothelial progenitor cells in patients with preeclampsia.
abstract: BACKGROUND
  In preeclampsia, the precise mechanism of impaired vascular function is still unclear. We hypothesized that cellular function of circulating endothelial progenitor cells (EPCs) might be impaired in patients with preeclampsia.
  
  
  OBJECTIVE
  The objective of this study was to investigate the number and status of cellular senescence of EPCs in the circulation of women with preeclampsia.
  
  
  METHODS
  Circulating EPCs were cultured from patients with preeclampsia (n = 8) and normotensive pregnant women (n = 7). EPC numbers were assessed by colony-forming unit (CFU) methodology as previously reported. In addition, to assess cellular senescence, we measured endogenous beta-galactosidase activity. Moreover, we assessed whether the serum level of C-reactive protein (CRP), a marker for systemic inflammation, was associated with cellular impairment of EPCs.
  
  
  RESULTS
  The number of circulating EPCs was decreased in women with preeclampsia controls (median, 10.0 vs. 34.0 CFU; P < 0.01). The rate of cellular senescence was significantly increased in patients with preeclampsia (33.9%) compared with that in controls (22.9%; P < 0.05). Patients with preeclampsia were divided into two subgroups: the CRP-negative group (CRP, <0.1 mg/dl; n = 4) and the CRP-positive group (CRP, > or =0.1 mg/dl; n = 4). Interestingly, EPC CFU counts were markedly decreased in CRP-positive patients compared with those in CRP-negative patients (5.0 and 25.0 CFU, respectively; P < 0.05). Median values for cellular senescence were greater in the CRP-positive group than in the CRP-negative group, although this did not achieve statistical significance (43.5% and 33.3%, respectively; P = 0.12).
  
  
  CONCLUSIONS
  Depletion and cellular aging of EPCs in patients with preeclampsia might be associated with endothelial dysfunction and could be affected by systemic inflammation.
authors.affiliation: Division of Maternal Fetal Medicine, Department of Obstetrics and Gynecology, Tohoku University Graduate School of Medicine, 1-1 Seiryomachi, Aobaku, Sendai 980-8574, Japan. sugawara@mail.tains.tohoku.ac.jp
authors.forename: Junichi
authors.initials: J
authors.lastname: Sugawara
authors.forename: Minori
authors.initials: M
authors.lastname: Mitsui-Saito
authors.forename: Chika
authors.initials: C
authors.lastname: Hayashi
authors.forename: Tetsuro
authors.initials: T
authors.lastname: Hoshiai
authors.forename: Masato
authors.initials: M
authors.lastname: Senoo
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Chisaka
authors.forename: Nobuo
authors.initials: N
authors.lastname: Yaegashi
authors.forename: Kunihiro
authors.initials: K
authors.lastname: Okamura
mesh_terms: D000328:Adult; D002097:C-Reactive Protein / Q000378:metabolism; D016022:Case-Control Studies; D002478:Cells, Cultured; D016922:Cellular Senescence; D003114:Colony-Forming Units Assay; D042783:Endothelial Cells / Q000473:pathology*; D005260:Female; D006801:Humans; D011225:Pre-Eclampsia / Q000097:blood* / Q000473:pathology*; D011247:Pregnancy; D013234:Stem Cells / Q000473:pathology*
chemical_list: D002097:C-Reactive Protein