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Decrease and dysfunction of endothelial progenitor cells in umbilical cord blood with maternal pre‐eclampsia
Author(s) -
Xia Liang,
Zhou Xin P.,
Zhu Jun H.,
Xie Xu D.,
Zhang Hao,
Wang Xing X.,
Chen Jun Z.,
Jian Sun
Publication year - 2007
Publication title -
journal of obstetrics and gynaecology research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.597
H-Index - 50
eISSN - 1447-0756
pISSN - 1341-8076
DOI - 10.1111/j.1447-0756.2007.00555.x
Subject(s) - vasculogenesis , medicine , andrology , soluble fms like tyrosine kinase 1 , umbilical cord , preeclampsia , cord blood , angiogenesis , eclampsia , fetus , endothelial progenitor cell , progenitor cell , umbilical vein , neovascularization , immunology , vascular endothelial growth factor , in vitro , placental growth factor , biology , stem cell , pregnancy , microbiology and biotechnology , vegf receptors , biochemistry , genetics
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. Result: 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/×200 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. Conclusion: 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.