子痫前期（PE）是一种妊娠期特发疾病。滋养细胞（EVT）功能表型的改变与PE发病密切相关。PDIA3P1是由芯片筛选、显著低表达于PE组织的假基因来源lncRNA。前期工作发现，沉默PDIA3P1可改变EVT功能表型；转录组测序提示调控EVT功能表型的关键因子核心蛋白聚糖（DCN）是PDIA3P1的下游靶基因；借助RNA蛋白预测及RIP实验，发现PDIA3P1与组蛋白去甲基化酶JMJD2A存在结合位点，且两者的相互作用参与调控DCN。故提出假基因PDIA3P1通过绑定JMJD2A调控DCN表达影响PE中EVT表型的科学假说。本研究拟阐明PDIA3P1的生物学特征；结合体内外多种环境，采用交叉过表达/沉默策略，研究假基因PDIA3P1通过JMJD2A在表观遗传水平调控DCN的分子机制。以PDIA3P1为切入点，将进一步揭示PE复杂病理发展的分子机制细节，并为PE的防治提供新线索和潜在新靶标。

Preeclampsia (PE) is known as a pregnancy-specifc disease. There is a close correlation between the functional phenotype changes of trophoblast and the pathogenesis of PE. Pseudogene PDIA3P1 was significantly down-regulated in PE tissues via high-through microarray detection. The earlier research revealed that silence of PDIA3P1 could change the normal functional phenotype of trophoblast. Transcriptome sequencing suggested that decorin (DCN), the key factor to regulate EVT functional phenotype, might be a candidate target gene of PDIA3P1. With the help of RNA-protein prediction and RIP experiments, we obtained that the Jumonji domain-containing protein 2A (JMJD2A), a histone demethylase, had binding sites with PDIA3P1, and the interaction of the two participated in the regulation of the expression of DCN. Therefore, we hypothesize that pseudogenes PDIA3P1 could regulate the expression of DCN by recruiting and binding JMJD2A to regulate the EVT phenotype in PE. This study intends to clarify the biological characteristics of PDIA3P1 at first. After that, using the cross over expression / silence strategy combined with experiments in vivo and in vitro, we propose to study the specific molecular mechanism of the regulation of DCN expression at the epigenetic level by pseudogenes PDIA3P1 through recruiting JMJD2A. Taking PDIA3P1 as the breakthrough point, the project shall further reveal the molecular mechanism details of PE complex pathological development, and may provide new clues and potential new targets for the prevention and treatment of PE.