Placental cell turnover in health and disease

Abstract

Pre-eclampsia (PE) and intra-uterine growth restriction (IUGR) cause significant maternal and perinatal morbidity and mortality. Placental dysfunction is central to the development of both conditions. Although the pathophysiology of these conditions is unknown, there is common placental pathology with an increase in apoptotic cell death seen within the trophoblast. In addition, in pre-eclampsia, apoptotic fragments of syncytiotrophoblast have been detected in the maternal circulation. Both hypoxia and reactive oxygen species have been proposed as potential mediators of the insults to the placenta in pre-eclampsia and IUGR resulting in apoptosis. Cell proliferation and apoptosis are tightly regulated by oncoproteins. The increased apoptosis observed within trophoblast is associated with an alteration in oncoprotein expression within placental tissue. Further investigation of these oncoproteins capable of detecting or responding to cell damage may improve understanding of the pathophysiology of pre-eclampsia and IUGR.