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

PPARy靶基因和细胞滋养层细胞融合在正常和病理胎盘中的作用，如先兆子痫、HELLP综合征和胎儿生长受限。

• 批准号: 5439368
• 负责人: Professor Dr. Ralf L. Schild
• 金额: --
• 依托单位: Klinik für Geburtshilfe und Perinatalmedizin
• 依托单位国家: 德国
• 项目类别: Research Grants
• 财政年份: 2004
• 资助国家: 德国
• 起止时间: 2003-12-31 至 2010-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/5439368?language=en
• 关键词: Die; Rolle; der; PPARy; Zielgene

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.

该提案解决了胎儿生长受限（FGR）和先兆子痫（PE）的重要临床问题。通过超声和多普勒超声评估的FGR和PE的存在或不存在将代表自变量，细胞和分子生物学技术为因变量。关于PPARg活性的可用数据强烈表明，胎盘PPARg的缺乏是PPARg -/-小鼠中滋养层分化和功能严重破坏的基础。重要的是，最近的证据已经发现，p38 a是小鼠和人滋养层细胞中PPARg活性的重要上调因子，特异性p38 ct抑制剂导致PPARg活性和滋养层分化的显著降低。我们推测，异常的基因表达水平的p38 ct和PPARg存在于异常胎盘与胎儿生长迟缓和PE的婴儿。本研究的目的是将以前在正常足月胎盘中的发现扩展到足月妊娠（对照组）和并发FGR和PE（研究组）的胎盘，以进一步研究PPARg和p38 ot在胎盘发育中的作用。