Preeclampsia (PE) is one of the mainly caused maternal and infant incidences and mortalities worldwide. However, the mechanisms underlying PE remained largely unclear. The present study identified 1716 high expressions of gene and 2705 low expressions of gene using GSE60438 database, and identified 7087 hypermethylated and 15120 hypomethylated genes in preeclampsia using GSE100197. Finally, 536 upregulated genes with hypomethylation and 322 downregulated genes with hypermethylation were for the first time revealed in PE. Gene Ontology (GO) analysis revealed that these genes were associated with peptidyl-tyrosine phosphorylation, skeletal system development, leukocyte migration, transcription regulation, T cell receptor and IFN-γ-involved pathways, innate immune response, signal transduction, cell adhesion, angiogenesis, and hemopoiesis. Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis demonstrated that aberrantly methylated differentially expressed genes were involved in regulating adherens junction, pluripotency of stem cell regulation, immune processing, T cell receptor and NF-κB pathways, HTLV-I and HSV infections, leishmaniasis, and NK-induced cytotoxicity. Protein-protein interaction (PPI) network analysis identified several hub networks and key genes, including MAPK8, CCNF, CDC23, ABL1, NF1, UBE2E3, CD44, and PIK3R1. We hope these findings will draw more attention to these hub genes in future PE studies.

中文翻译：

---

先兆子痫差异表达及甲基化基因综合分析

先兆子痫（PE）是世界范围内主要引起的母婴发病率和死亡率之一。然而，PE 的潜在机制在很大程度上仍不清楚。本研究利用GSE60438数据库鉴定了1716个高表达基因和2705个低表达基因，利用GSE100197鉴定了先兆子痫7087个高甲基化基因和15120个低甲基化基因。最后，在PE中首次揭示了536个低甲基化上调基因和322个高甲基化下调基因。基因本体论 (GO) 分析显示，这些基因与肽基酪氨酸磷酸化、骨骼系统发育、白细胞迁移、转录调控、T 细胞受体和 IFN- γ 相关- 涉及的通路、先天免疫反应、信号转导、细胞粘附、血管生成和造血。京都基因与基因组百科（KEGG）通路分析表明，异常的甲基化差异表达基因，参与调节粘着连接，干细胞调节，免疫处理，T细胞受体和NF-的多能性κ乙通路，HTLV-I和HSV感染、利什曼病和 NK 诱导的细胞毒性。蛋白质-蛋白质相互作用 (PPI) 网络分析确定了几个枢纽网络和关键基因，包括 MAPK8、CCNF、CDC23、ABL1、NF1、UBE2E3、CD44 和 PIK3R1。我们希望这些发现将在未来的 PE 研究中引起对这些枢纽基因的更多关注。