Decrease and dysfunction of endothelial progenitor cells in umbilical cord blood with maternal pre-eclampsia.
BACKGROUND
The pre-eclampsia is characterized by placental defective angiogenesis and maternal vascular/endothelial dysfunction. Recently, the decrease and senescence of endothelial progenitor cells (EPC) has been observed in maternal circulation with pre-eclampsia. Given the essential involvement of EPC in neovascularization and reendothelialization, we investigate whether or not the depletion of EPC is existent in placental/fetal circulation with maternal pre-eclampsia.


METHODS
Samples of venous cord blood were collected during the labor of preeclamptic mothers (n = 14) and normotensive controls (n = 10). Circulating EPC were enumerated as AC133+/KDR+ cells via fluorescence-activated cell sorting (FACS) analysis. Additionally, EPC were expanded in vitro and identified by DiI-acLDL uptake and lectin staining by direct fluorescent staining under a laser scanning confocal microscope. EPC proliferation, migration and vasculogenesis activities were determined by MTT, modified Boyden chamber assay and in vitro vasculogenensis assay.


RESULTS
The placental/fetal circulating EPC numbers were significantly decreased in the pre-eclampsia group compared with the control (median, 200; range, 100-440 cells/mL vs 390; 270-440 cells/mL, P < 0.001), and after in vitro cultivation the numbers of EPC also decreased in pre-eclampsia group (19.5; 5.0-32.0 vs 39.5; 31.2-52.0 EPC/x200 field; P < 0.001). Both circulating EPC and cultivated EPC were inversely correlated with cord blood level of soluble fms-like tyrosine kinase 1 (sFlt-1). In addition, the EPC from patients with pre-eclampsia were significantly impaired in their proliferation, migration and vasculogenesis capacities.


CONCLUSIONS
The present study documented the decrease and dysfunction of placental/fetal circulating EPC in patients with pre-eclampsia. The alteration is probably associated with the increased sFlt-1 levels in the umbilical cord blood.
Xia
Liang
L
Department of Cardiovascular Diseases, the First Affiliated Hospital, Medical School of Zhejiang University, Hangzhou, China.
Zhou
Xin P
XP
Zhu
Jun H
JH
Xie
Xu D
XD
Zhang
Hao
H
Wang
Xing X
XX
Chen
Jun Z
JZ
Jian
Sun
S
D000328:Adult; D048708:Cell Growth Processes; D002465:Cell Movement; D016207:Cytokines / Q000097:blood; D042783:Endothelial Cells / Q000473:pathology*; D005260:Female; D005312:Fetal Blood / Q000166:cytology*; D006801:Humans; D007231:Infant, Newborn; D008297:Male; D009389:Neovascularization, Pathologic / Q000473:pathology; D011225:Pre-Eclampsia / Q000097:blood* / Q000473:pathology; D011247:Pregnancy; D013234:Stem Cells / Q000166:cytology*
D016207:Cytokines