子痫前期滋养细胞侵袭力降低的机制不清。课题组发现RNA结合蛋白PTBP1在PE胎盘组织中低表达，与N-cadherin和Vimentin表达正相关；芯片检测发现circ_00296922表达下调；软件预测到circ_0029692 两端侧翼序列存在PTBP1 的结合位点。PTBP1是否能促进circ_0029692生成；circ_0029692能否结合miR-372-3p和miR-135b-5p，改变其对靶基因的调控；Twist1能否转录调控PTBP1形成反馈环路，调控EMT？有待阐明。项目拟明确PTBP1促进circ_0029692生成；circ_0029692结合miR-372-3p和miR-135b-5p，改变其对Twist1、N-cadherin和Vimentin的负性调控；Twist1转录调控PTBP1形成反馈环路，共同调控EMT的机制。为深入研究PE的发病机制提供新思路。

The mechanism of decreased invasiveness in preeclampsia trophoblast cells is not clear. Our team found RNA-binding protein PTBP1 exhibited low expression in PE placenta tissue, and its expression level was positively correlated with the expression of Vimentin and N-cadherin; Chip detection results proved the down-regulated expression of circ_0029692; Bioinformatics Software predicted there were binding sites between PTBP1 and both end flanking sequences of circ_0029692. Whether PTBP1 promotes the generation of circ_0029692, whether circ_0029692 combines with miR-135b-5p and miR-372-3p thus altering regulation of its target genes, and whether Twist1 facilitates the transcriptional regulation on PTBP1 and form a feedback loop, consequently regulating epithelial to mesenchymal transition remained to be expounded. This project explicitly showed that PTBP1 could promote the generation of circ_0029692; Circ_0029692 could combine with miR-372-3p and miR-135b-5p thus altering its negative regulation on TWIST1, N-cadherin and Vimentin; Twist1 could facilitate the transcriptional regulation on PTBP1, forming feedback loop and controling EMT of PE trophoblast cells. The project will provide a new approach for further research on the pathogenesis of PE.