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Identifier

000382540

Title

Ο ρόλος των νευροπεπτιδίων CRF και UCN στην παθοφυσιολογία της διείσδυσης της εξωλαχνωτής τροφοβλάστης κατά την πλακουντοποίηση.Διερεύνηση της συμμετοχής των μορίων αυτών στην παθογένεση νόσων με ελαττωματική πλακουντοποίηση, όπως η προεκλαμψία

Alternative Title

The role of neuropeptides CRF and UCN in the pathophysiology of extravillous trophoblast invasion during placentation .Investigation of these molecules involvment in the pathogenesis of diseases associated with defective placentation ,like preeclampsia

Author

Πέτσας, Γεώργιος

Reviewer

Μακρυγιαννάκης, Αντώνιος

Reviewer

Μαυροθαλασσίτης, Γεώργιος
Τσατσάνης, Χρήστος
Ζηκόπουλος, Κων/νος
Μακρυδήμας, Γεώργιος
Ρελάκης, Κων/νος
Παπακωνσταντή, Ευαγγελία

Abstract

Corticotropin-releasing factor (CRF) and its receptors are expressed in human placenta. Recently impaired function of this system has been associated with a number of complications of pregnancy, including preeclampsia. The aim of the study was to test the hypothesis that CRF participates in the pathophysiology of preeclampsia through induction of macrophage-mediated apoptosis of extravillous trophoblasts (EVT). We found that expression of CRF was increased in EVT of placental bed biopsy specimens from preeclamptic pregnancies (1.8-fold increase; P΄&λτ0.05). In addition, significantly higher numbers of apoptotic EVT were detected in preeclamptic placentas compared to normal ones (P΄&λτ0.05) and only in preeclamptic placentas decidual macrophages were found to be FasL positive. In vitro studies on the effect of CRF on human macrophages suggested that CRF induced the expression of FasL protein in human macrophages and potentiated their ability to induce apoptosis of a Fas-expressing EVT-based hybridoma cell-line in cocultures. Theses findings demonstrate a possible mechanism by which aberrant expression of CRF in preeclampsia may activate FasL positive decidual macrophages, impair the physiological turnover of EVT and eventually disturb placentation

Language

Greek

Subject

Apoptosis

Cortocotropin-releasing factor

Extravillous trophoblast

FAS ligand

FAS receptor

Macrophage

Placentation

Preeclampsia

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