The placenta in preeclampsia

Abstract

The root cause of preeclampsia is the placenta. Preeclampsia begins to abate with the delivery of the placenta and can occur in the absence of a fetus but with the presence of trophoblast tissue with hydatidiform moles. In view of this, study of the placenta should provide insight into the pathophysiology of preeclampsia. In this presentation we examine placental pathological and pathophysiological changes with preeclampsia and fetal growth restriction (FGR). It would seem that this comparison should be illuminating as both conditions are associated with similarly abnormal placentation yet only in preeclampsia is there a maternal pathophysiological syndrome. Similar insights about early and late onset preeclampsia should also be provided by such information. We report that the placental abnormalities in preeclampsia are what would be predicted in a setting of reduced perfusion and oxidative stress. However, the differences from FGR are inconsistent. The most striking differences between the two conditions are found in areas that have been the least studied. There are differences between the placental findings in early and late onset preeclampsia but whether these are qualitative, indicating different diseases, or simply quantitative differences within the same disease is difficult to determine. We attempt to decipher the true differences, seek an explanation for the disparate results and provide recommendations that we hope may help resolve these issues in future studies.

Adenosine A2A receptor regulates expression of vascular endothelial growth factor in feto-placental endothelium from normal and late-onset pre-eclamptic pregnancies

“…Then, even increased angiogenesis observed in LOPE may be insufficient to overcome both the reduced oxygen delivery that is due to the infarcted placenta and the reduced oxygen delivery that would be predicted with failed remodeling of the maternal spiral arteries supplying the intervillous space [32]. More work is needed to better assess the role of hypoxia in the increased placental angiogenesis present in LOPE.…”

Impaired A2A adenosine receptor/nitric oxide/VEGF signaling pathway in fetal endothelium during late- and early-onset preeclampsia

“…Preeclampsia is characterized by placental insufficiency, mainly during early onset [8], which has been associated with low placental angiogenesis [3,4,6,28]. We have studied the cell proliferation/migration of HUVECs as the initial steps linked with angiogenesis.…”

“…We are trying to overcome this limitation through the inclusion of detailed clinical characteristics of the included patients. In fact, we have suggested [3] that it is necessary to include as much clinical data as possible in order to facilitate the interpretation of the results presented in studies including preeclamptic patients.…”

“…There is significant evidence linking the genesis of preeclampsia and its associated perinatal outcomes with placental alterations, as we have recently reviewed [3]. One of the main features in the placenta from a preeclamptic pregnancy is failure of spiral artery remodeling, a phenomenon linked not only with reduced maternal blood flow toward the placenta [4] but also with high velocity and pressure of maternal inflow that may impair the placental villous structure [5].…”

“…In particular, microarray analysis has described the lower expression of at least two angiogenesis-associated transcripts (Egfl7 and Acvrl1) in EOPE compared to LOPE or agematched controls [15]. Therefore, reduced placental angiogenesis could be responsible for the impaired placental blood flow observed in EOPE, while the observed normal blood flow in LOPE could result from either no alterations or increased placental angiogenesis [3,6,13].…”