Die Rolle der PPARy Zielgene und der Zell-Zellfusion von Zytotrophoblasten in normalen und pathologischen Plazenten, wie Preeklamspie, HELLP-Syndrom und fötaler Wachstumsrestriktion.

点击翻译按钮获取中文摘要

The proposal addresses the important clinical problem of fetal growth restriction (FGR) and preeclampsia (PE). Presence or absence of FGR and PE as assessed by ultrasound and Doppler sonography will represent the independent variable, techniques in cellular and molecular biology the dependent variable. The data available on PPARg activity strongly suggest that the lack of placental PPARg underlies the profound disruption of trophoblast differentiation and fimction in PPARg -/- mice. Importantly, recent evidence has found p38a to be an important up-regulator of PPARg activity in murine and human trophoblasts with specific p38ct inhibitors leading to a marked decrease of PPARg activity and trophoblast differentiation. We hypothesize that aberrent gene expression levels of both p38ct and PPARg exist in abnormal placentas from babies with FGR and PE. The study aim is to extend previous findings in normal term placentas to placentas from pregnancies delivered remote from term (control group) and complicated by FGR and PE (study group) to further examine the role of PPARg and p38ot in placental development.