Models of pre-eclampsia European researchers investigated the underlying molecular cause of pre-eclampsia to address the great medical need for therapies. Health © Artemida-psy, Shutterstock Pre-eclampsia is a pregnancy complication associated with high blood pressure and signs of kidney damage. One of the primary causes of pre-eclampsia is the disruption of proteins, which control new blood vessel growth. However, therapies are restricted by the ability to experimentally model the clinical symptoms. To address this issue, the EU-funded IVSCP (Knowledge Transfer of in vivo surgery and cardiovascular phenotyping for angiogenesis and preeclampsia studies) project set out to develop experimental disease models through application of cutting edge in vivo techniques. The key objective was to transfer expertise in cardiovascular microsurgery and background in effectively phenotyping cardiovascular disease in transgenic mouse models. Accumulating evidence indicates a role for the anti-angiogenic soluble Flt-1 (sFlt-1) and angiogenic placenta growth factor (PlGF) in pre-eclampsia. To complement existing knowledge, IVSCP researchers set out to assess glutaredoxin-1 as a therapeutic target of pre-eclampsia and to identify the regulators of sFlt-1in angiogenesis. Furthermore, they investigated the function of PIGF in the endothelium and worked to identify novel redox-sensitive targets implicated in pre-eclampsia. In this context, they employed various models of left ventricular hypertrophy and endothelial mesenchymal transition, and isolated cardiac microvascular endothelial cells for further characterisation. They also used laser Doppler to monitor blood flow recovery and implanted telemeters in mice for blood pressure measurement. Apart from the research activities, considerable effort during the IVSCP study went into the transfer of knowledge to the host institution and to the laboratory training of undergraduate and graduate students. Keywords Pre-eclampsia, IVSCP, phenotyping, angiogenesis, sFlt-1, placenta growth factor
