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子痫前期差异表达和甲基化基因的综合分析。

Comprehensive Analysis of Differently Expressed and Methylated Genes in Preeclampsia.

机构信息

Department of Obstetrics and Gynecology, Tongren Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200032, China.

Department of Obstetrics and Gynecology, Kongjiang Hospital, Shanghai 200093, China.

出版信息

Comput Math Methods Med. 2020 Nov 1;2020:2139270. doi: 10.1155/2020/2139270. eCollection 2020.

Abstract

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--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-B 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.

摘要

子痫前期 (PE) 是全球主要导致母婴发病率和死亡率的疾病之一。然而,PE 的发病机制仍不清楚。本研究通过 GSE60438 数据库鉴定出 1716 个高表达基因和 2705 个低表达基因,并通过 GSE100197 鉴定出 7087 个超甲基化基因和 15120 个低甲基化基因。最后,首次在 PE 中发现了 536 个低甲基化的上调基因和 322 个高甲基化的下调基因。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 相关途径、固有免疫反应、信号转导、细胞黏附、血管生成和造血有关。京都基因与基因组百科全书 (KEGG) 通路分析表明,异常甲基化的差异表达基因参与调节黏附连接、干细胞调节的多能性、免疫加工、T 细胞受体和 NF-B 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。我们希望这些发现能在未来的 PE 研究中引起更多人对这些枢纽基因的关注。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5b39/7652635/4d2d03d28e50/CMMM2020-2139270.001.jpg

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