Líffræðifélag Íslands - biologia.is
Líffræðiráðstefnan 2021
Erindi/veggspjald / Talk/poster E71
Höfundar / Authors: Hallfríður Ingólfsdóttir (1), Guðrún Valdimarsdóttir (1), Marta S. Alexdóttir (1), Þóra Steingrímsdóttir (2)
Starfsvettvangur / Affiliations: 1. University of Iceland, 2. Landspitali University Hospital
Kynnir / Presenter: Hallfríður Ingólfsdóttir
Preeclampsia (PE) is a severe pregnancy disease believed to originate in the placenta. It is the leading cause of maternal/fetal mortality worldwide and there is no cure for severe PE except delivery of the baby and placenta. During normal placental development, trophoblasts (TBs) invade the maternal spiral arteries to replace the endothelial lining which widens the vessel and enables sufficient flow of nutrients to the fetus. In PE this invasion seems to fail which can lead to inadequate flow to the placenta. The underlying mechanisms responsible for PE are not well understood. However, studies suggest that the dysregulation and imbalance of certain angiogenic factors in the placenta could be the cause of PE. The Transforming growth factor-beta (TGF-b) family plays an important role in placentation, yet studies show contradicting results. TGF-b and Bone morphogenetic proteins (BMPs) bind to specific ALK receptors which activate SMAD transcription factors, leading to either anti- or pro-angiogenic activity. Our preliminary data suggest that the TGF-b family is signalling through opposing signalling cascades to regulate TB invasion. With in vitro studies on TBs and biological samples from women with PE, our studies aim to define the mechanisms of these pathways. In addition, we want to characterize the roles of the different components of the two TGF-b superfamily cascades which could be used for molecular targeting for prediction and prevention of PE.