The effect of labour and placental separation on the shedding of syncytiotrophoblast microparticles, cell-free DNA and mRNA in normal pregnancy and pre-eclampsia.
The clinical features of the maternal syndrome of pre-eclampsia can be explained by generalised maternal endothelial cell dysfunction, which is a part of a more global maternal systemic inflammatory response. There is growing evidence that these effects are associated with the shedding of cellular debris, including syncytiotrophoblast microparticles (STBM), cell-free DNA and mRNA, from the surface of the placenta (syncytiotrophoblast) into the maternal circulation. The increased shedding of this debris seen in pre-eclampsia is believed to be caused by placental ischaemia, reperfusion and oxidative stress. This study was carried out to determine whether uterine contractions during labour and subsequent placental separation lead to an acute increase in the release of placental debris into the maternal circulation. To assess the effects of labour, samples were taken from 10 normal pregnant (NP) and 10 pre-eclamptic (PE) women at varied time points. Similarly to assess the effects of placental delivery, plasma samples were taken from 10 NP and 10 PE women undergoing elective caesarean section. There was a significant increase in the shedding of STBM in pre-eclampsia which was not seen in normal pregnancy and there was a small rise in STBM levels at placental separation in both normal pregnant and pre-eclamptic women undergoing caesarean section, but the differences were not significant. However, levels of placental cell-free corticotrophin releasing hormone mRNA were significantly increased in labour in both normal pregnancy and pre-eclampsia and were still high 24 h after delivery in the pre-eclamptic women. There was no significant increase in fetal or total DNA in labour, but the overall levels of total DNA (maternal and fetal) was increased in labour in pre-eclampsia compared to normal labour. The enhanced shedding of STBM and CRH mRNA in pre-eclampsia labour may have a role in cases of postpartum worsening of pre-eclampsia.
Reddy
A
A
Nuffield Department of Obstetrics and Gynaecology, Level 3, Women's Centre, John Radcliffe Hospital, Oxford OX3 9DU, UK.
Zhong
X Y
XY
Rusterholz
C
C
Hahn
S
S
Holzgreve
W
W
Redman
C W G
CW
Sargent
I L
IL
D000328:Adult; D002585:Cesarean Section; D004247:DNA / Q000097:blood; D005260:Female; D006801:Humans; D007743:Labor, Obstetric / Q000502:physiology*; D010316:Particle Size; D011225:Pre-Eclampsia / Q000097:blood* / Q000473:pathology* / Q000503:physiopathology; D011247:Pregnancy; D012333:RNA, Messenger / Q000097:blood; D014327:Trophoblasts / Q000473:pathology* / Q000502:physiology*
D012333:RNA, Messenger; D004247:DNA