Recent morphologic studies of preeclampsia-affected placentas have shown irregular and narrow lumina on fetal placental capillary and increased branching angiogenesis in chorionic villi. Depletion and functional impairment of circulating endothelial progenitor cell (EPC) is associated with diseases related to endothelial dysfunction. The aim of this study is to investigate the number and functional status of fetal EPCs in pregnancies complicated by preeclampsia without intrauterine growth restriction (IUGR).
Fetal EPCs were isolated, characterized, and counted from 17 women with preeclampsia without IUGR and 30 gestational age-matched normotensive pregnant women. After ex vivo cultivation and differentiation, colony forming assay and differentiation time assay were performed to detect functional activity of the cells. In addition, to assess cellular senescence, senescence-associated β-galactosidase (SA-β-gal) staining for EPCs was executed and the staining density was detected by densitometry.
The number of circulating fetal EPCs was significantly lower in the preeclamptic pregnancy compared with normal pregnancy (6.3 ± 2.2 vs. 4.1 ± 1.8×105/50ml, p<0.001). Compared with normal pregnancy, differentiation time from EPC to outgrowing cell was longer (p<0.001), and the number of colonies after differentiation was smaller in preeclampsia (p<0.001). The intensity of SA-β-gal staining was higher in preeclamptic pregnancy (p<0.001).
This study shows that the number and functional ability of fetal EPCs in pregnancies complicated by preeclampsia are significantly decreased and more senescent compared to those of normal pregnancy. Such impairment may be associated with fetal endothelial dysfunction. And these alterations of fetal EPCs may give an explanation for placental dysfunction in preeclamptic condition.
© 2007 Mosby, Inc. Published by Elsevier Inc. All rights reserved.