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Circulating endothelial progenitor cells during normal pregnancy and pre-eclampsia
Keiichi Matsubara1, Emiko Abe, Yuko Matsubara
1Department of Obstetrics and Gynecology, Ehime University School of Medicine, Japan. keiichi@m.ehime-u.ac.jp
Insights
Endothelial progenitor cell (EPC) proliferation is increased in pre-eclampsia (PE), despite similar cell numbers. Angiotensin II and TNF-alpha stimulate EPC proliferation in PE, suggesting a role in utero-placental circulation disturbances.
Area of Science:
- Reproductive biology
- Vascular biology
- Cellular biology
Background:
- Endothelial progenitor cells (EPCs) are crucial for neovascularization in the uterine endometrium and utero-placental circulation.
- Pre-eclampsia (PE) is a pregnancy complication characterized by impaired utero-placental circulation.
Purpose of the Study:
- To investigate differences in EPC proliferation between normal pregnancy and pre-eclampsia.
- To determine the role of Angiotensin II (Ang II) and Tumor Necrosis Factor-alpha (TNF-alpha) in EPC proliferation in PE.
Main Methods:
- Quantified peripheral blood EPC numbers using flow cytometry in non-pregnant, normal pregnant, and PE groups.
- Assessed EPC proliferation via acetylated LDL uptake and lectin binding after 7-day culture.
- Measured EPC proliferative activity induced by Ang II and TNF-alpha using BrdU assay.
Main Results:
- No significant difference in peripheral blood EPC numbers between PE and normal pregnancy groups.
- Significantly increased EPC proliferation observed in patients with PE compared to normal pregnancy.
- Ang II and TNF-alpha demonstrably induced proliferation of EPCs from PE patients.
Conclusions:
- While EPC proliferation is enhanced in PE, potentially stimulated by factors like Ang II and TNF-alpha, impaired EPC mobilization may hinder EC regeneration.
- Serum factors might impair EPC mobilization, contributing to insufficient EC regeneration in the disturbed utero-placental circulation of PE.
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-alpha (TNF-alpha) 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-alpha induced the proliferation of EPC derived from patients with PE.
Conclusions:
In PE, some factors including Ang II and TNF-alpha 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.
