Placental bed apoptosis is increased in pregnant women with pre-eclampsia versus normotensive pregnant women

Abstract

We hypothesised that apoptosis in the placenta is increased in pregnant women whose pregnancies were complicated by pre-eclampsia as compared to normal pregnant women. Biopsy samples were obtained by punch biopsy from placental beds in 15 pre-eclamptic and 15 normotensive pregnant women during cesarean section. Apoptosis in syncytiotrophoblasts, syncytial cluster, extravillous cytotrophoblast, and decidual and stromal cells were evaluated by caspase-3, bax and terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end-labelling (TUNEL) immunohistochemical methods. A significant involvement was observed via caspase-3 and TUNEL methods in the syncytiotrophoblasts, syncytial cluster and extravillous cytotrophoblast cells of the pre-eclamptic group versus normotensive group (p < 0.001). Caspase-3 method found significantly increased involvement in the pre-eclamptic group versus normotensive group (p < 0.001). Although bax method found significantly increased involvement in syncytiotrophoblasts in the pre-eclamptic group versus normotensive group (p < 0.001), no significant difference was found between the groups in terms of involvement of other cell groups (p > 0.05). Apoptosis in the placental bed is increased in pre-eclamptic woman.

Anti-Apoptotic Effect of Apelin in Human Placenta: Studies on BeWo Cells and Villous Explants from Third-Trimester Human Pregnancy

“…Similarly, the levels of protein of caspase 3, 8 and 9 as well as p53 were lower; they were also time-and dose-dependent. In many placentas from complicated pregnancies, pathologies have been observed with significantly higher expressions of caspase 3 and p53 [10,12,42]. The inhibition of their expression by apelin has a positive effect on trophoblast cell survival.…”

“…Nevertheless, it is generally considered that apoptosis in the placenta of pregnancies complicated by pathologies, including preeclampsia, intrauterine growth restriction (IUGR) and miscarriage, occurs more frequently than in trophoblast cells from normal pregnancies. In placentas affected by these pathologies, the downregulation of BCL2 expression has been observed, along with higher expression levels of protein p53 and caspase 3 [11][12][13]. In general, apoptosis is mainly observed in the syncytial layer of the placenta, while it is rare in cytotrophoblast cells, possibly because the syncytiotrophoblast consists of the greater part of the placenta and its external part of the trophoblast is more sensitive to death signals [14,15].…”

Placenta Of Late Onset Preeclampsia Without Fetal Growth Restriction : Is It Different From The Normal?

“…This may be explained by the presence of a population of early onset PE in their study group [1,7,8] . Dagdelen et al, (2016), we have found significant increase in apoptotic activity in trophoblastic cells as highlighted by caspase 3 [6,[14][15][16][17][18] . This can suggest that whatever the time of onset of PE the pathogenetic mechanisms are nearly similar.…”

“…Such antiangiogenic substances (serum CD105) and inflammatory cytokines released into the maternal circulation can lead to systemic inflammatory response and endothelial dysfunction [5,6] .…”

FAS gene polymorphisms (rs3740286 and rs4064) were not associated with pre-eclampsia risk

“…It is, then, shown that hypoxia triggered apoptosis. Thus, increased apoptosis, seen in pre-eclampsia, does not seem to be the reason for trophoblastic invasion but an occasion of pathology developing secondary to it (Dagdelen et al 2016).…”