Does oxygen concentration affect shedding of trophoblastic debris or production of inflammatory mediators from first trimester human placenta?

Abstract

Preeclampsia is a major cause of pregnancy morbidity and mortality. It is hypothesised that necrotic syncytial knots and/or inflammatory factors released from the placenta into the maternal circulation are responsible for inducing the widespread endothelial cell activation that is seen in preeclampsia. Poor placental perfusion has been associated with preeclampsia, this had led to the hypothesis that placental hypoxia has an important role in the pathogenesis of preeclampsia. In this study, using a placental explant model, we investigated whether different oxygen environments induced abnormal shedding of trophoblastic debris or secretion of cytokines from the placenta. There was no significant difference in the numbers of trophoblasts shed from explants cultured in 1% or 8% oxygen containing environments. There was also no difference in the levels of activated caspases in trophoblasts shed from explants cultured in these two oxygen environments nor was there a significant difference in the endothelial cell responses to trophoblasts shed from explants cultured in 1% or 8% oxygen. Similarly, there was no significant change in the secretion of nine cytokines into the conditioned medium from explants cultured in 1% or 8% oxygen. This study supports the growing evidence that levels of oxygen in the placental environment during the first trimester of pregnancy may not in itself be the essential component contributing to the pathogenesis of preeclampsia.