Shedding of syncytiotrophoblast microvilli into the maternal circulation in pre-eclamptic pregnancies
Article first published online: 19 AUG 2005
BJOG: An International Journal of Obstetrics & Gynaecology
Volume 105, Issue 6, pages 632–640, June 1998
How to Cite
Knight, M., Redman, C. W. G., Linton, E. A. and Sargent, I. L. (1998), Shedding of syncytiotrophoblast microvilli into the maternal circulation in pre-eclamptic pregnancies. BJOG: An International Journal of Obstetrics & Gynaecology, 105: 632–640. doi: 10.1111/j.1471-0528.1998.tb10178.x
- Issue published online: 19 AUG 2005
- Article first published online: 19 AUG 2005
- Received 15 September 1997 Returnedfor revision 14 January 1998 Accepted 4 March 1998
Objective To investigate whether syncytiotrophoblast microvilli (STBM) are shed into the maternal circulation in increased amounts in pre-eclamptic pregnancies as a possible cause of maternal vascular endothelial dysfunction.
Design A time-resolved fluoroimmunoassay was developed to measure STBM levels in peripheral and uterine venous plasma from normal pregnant and pre-eclamptic women. Three colour flow cytometry was used to assess the microparticulate nature of the STBM in pregnancy plasma. The effects of these plasmas on endothelial cell proliferation was compared and a correlation with the levels of STBM detected was sought.
Setting A laboratory investigation using clinical samples obtained from an obstetric practice in a teaching hospital.
Samples Peripheral venous plasma from 20 women with established pre-eclampsia, 20 normal pregnant women matched for age, gestation and parity, and 10 nonpregnant women of reproductive age. Paired uterine and peripheral venous plasma taken at caesarean section from 10 women with pre-eclampsia and 10 unmatched normal pregnant women.
Results STBM were detected in the plasma of pregnant women by both flow cytometry and time-resolved fluoroimmunoassay. Significantly higher levels of STBM were found in women with established pre-eclampsia (P= 0.01). STBM concentrations were higher in uterine venous plasma than in concurrently sampled peripheral venous plasma, confirming their placental origin. A significant correlation was found between the amount of STBM in the plasma and endothelial cell inhibitory activity.
Conclusions STBM are shed into the maternal circulation (microvillous deportation) and are present in significantly increased amounts in pre-eclamptic women. They may contribute to the endothelial dysfunction underlying the maternal syndrome of pre-eclampsia.