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Circulating Endothelial Progenitor Cells During Normal Pregnancy and Pre‐Eclampsia
Author(s) -
Matsubara Keiichi,
Abe Emiko,
Matsubara Yuko,
Kameda Kenji,
Ito Masaharu
Publication year - 2006
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/j.1600-0897.2006.00387.x
Subject(s) - eclampsia , progenitor cell , pregnancy , preeclampsia , medicine , endothelial stem cell , progenitor , andrology , obstetrics , endocrinology , biology , immunology , stem cell , microbiology and biotechnology , biochemistry , genetics , in vitro
Problem Endothelial progenitor cell (EPC), which mediates neovascularization of uterine endometrium may be involved in the neovascularization in the utero‐placental circulation. We evaluated whether EPC proliferation in pre‐eclampsia (PE) differed from that in normal pregnancy. Method of study EPC number in peripheral blood (20 non‐pregnancy, 36 normal pregnancy, 10 PE) was measured using flow cytometry. Peripheral blood mononuclear cell was cultured for 7 days and EPC proliferation was assessed based on detection of the uptake of acetylated low‐density lipoprotein and lectin. Furthermore, the proliferative activity induced by angiotensin II (Ang II) and tumor necrosis factor‐ α (TNF‐ α ) was measured by BrdU assay. Results EPC number in peripheral blood did not differ significantly between PE and normal pregnancy; however, EPC proliferation was significantly increased in PE. Furthermore, Ang II and TNF‐ α induced the proliferation of EPC derived from patients with PE. Conclusions In PE, some factors including Ang II and TNF‐ α stimulated EPC proliferation; however, the impairment of EPC mobilization into systemic circulation by serum factors may contribute to insufficient regeneration of EC in disturbed utero‐placental circulation of PE.