Comprehensive Analysis of Differently Expressed and Methylated Genes in Preeclampsia

Xu, Wenyi and Ru, Ping and Gu, Zhuorong and Zhang, Ruoxi and Pang, Xixia and Huang, Yi and Liu, Zhou and Liu, Ming and Chen, Lei (2020) Comprehensive Analysis of Differently Expressed and Methylated Genes in Preeclampsia. Computational and Mathematical Methods in Medicine, 2020. pp. 1-10. ISSN 1748-670X

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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-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.

Item Type: Article
Subjects: Universal Eprints > Medical Science
Depositing User: Managing Editor
Date Deposited: 23 Dec 2022 03:56
Last Modified: 22 Jun 2024 07:56
URI: http://journal.article2publish.com/id/eprint/1098

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