P 29 Involvement of the placental neuropeptide system in preeclampsia

Introduction One of the causes of preeclampsia (PE) is due to an imbalance of inflammatory and anti-inflammatory proteins, as well as hyperactivity of the sympathetic nervous system. Previous studies have already revealed the involvement of the neuropeptides galanin (GAL) and oxytocin (OXT) in inflammatory processes and their modulatory role with respect to the autonomous system 1, 2. Despite those findings, evidence for a relation of these hormones in the pathogenesis of PE is missing so far. Objectives Aim of the study is to characterise the above mentioned peptide systems regarding their expression patterns in the placenta, umbilical cord and plasma of PE patients and healthy controls. Patients and methods Placental (maternal and fetal side) and umbilical cord tissues have been collected during caesarean section from control and PE patients. Furthermore blood samples have been taken at the day of the surgery and four days postpartum. Biopsies have been analysed for the expression of GAL, GAL1,3- and OXT-receptors (GAL1, GAL3, OXTR). Additionally, differentiated analysis of maternal and fetal tissue was performed to reveal potential different expression patterns. Results Preliminary results of the IHC revealed a clear expression of GAL3 in trophoblasts of PE placentas, whereas controls showed an increase expression of GAL3 on endothelial cells. Moreover an increased expression of GAL1 and GAL on endothelial cells has been detected in controls compared to PE. Different patterns were also visible regarding the OXTR with higher expression levels in controls compared to PE. Furthermore, PE placentas showed local expression differences (fetal > maternal side), which was not apparent in controls. Conclusion The different expression patterns of the GAL-system and the OXTR still have to be verified by Western Blot analyses, qPCR and IHC. However, their preliminary detection in placental tissue could be a first hint regarding the involvement of those systems in the inflammatory processes of PE.