滋养层细胞浸润不足，胎盘血管生成异常是子痫前期的重要病理表现。人滋养层细胞内，Fibrillin 2 经Furin酶切可释放一种新多肽—Placensin；血清Placensin水平随妊娠进展显著升高。孕早期Placensin高表达于细胞滋养层细胞，Placensin可增加滋养层细胞浸润，且子痫前期患者血清Placensin水平显著低于正常对照组。基于这些研究，我们提出以下假说，Placensin调控滋养层细胞浸润和血管生成，Placensin分泌不足导致子痫前期。本课题组以人原代滋养层细胞和HTR-8/SVneo细胞系为研究对象，探究滋养层细胞内Placensin生成的调控机制;通过纯化哺乳动物重组Placensin，系统研究Placensin对人滋养层细胞浸润和血管生成的调控作用和机制。本研究将阐明子痫前期发生过程中Placensin的作用机制，为其作为子痫前期预测指标提供理论基础。

Insufficient trophoblast cell invasion and abnormal angiogenesis in placenta have been characterized as major factors that contribute to the pathogenesis of pre-eclampsia. Pro-fibrillin 2 (pro-FBN2) can generate placensin, a glucogenic peptide, following furin cleavage at the C-terminus of pro-FBN2. Serum Placensin level increased in stage-dependent manner. Our previous studies showed that, Placensin is highly expressed in cytotrophoblasts and could promote the invasiveness of trophoblasts, wheares serum Placensin level is lower in pre-eclampsia patients than normal prenancies. Based on above results, we bring up the following hypotheses, Placensin could promote trophoblast invasiveness and angiogenesis, while the insufficient Placensin secretion may lead to pre-eclampsia. To test these hypotheses, we will purify mammalian recombinant Placensin, and investigate its regulatory role on human trophoblast invasiveness and angiogenesis. Current study will interpret the role Placensin played during the onset of pre-eclampsia, which will provide mechanism evidence for Placensin as a serum marker for the prediction of pre-eclampsia.