Analysis of key genes and their functions in placental tissue of patients with gestational diabetes mellitus

This study was aimed at screening out the potential key genes and pathways associated with gestational diabetes mellitus (GDM). The GSE70493 dataset used for this study was obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) in the placental tissue of women with...

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Published inReproductive biology and endocrinology Vol. 17; no. 1; p. 104
Main Authors Wang, Yuxia, Yu, Haifeng, Liu, Fangmei, Song, Xiue
Format Journal Article
LanguageEnglish
Published England BioMed Central Ltd 29.11.2019
BioMed Central
BMC
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Summary:This study was aimed at screening out the potential key genes and pathways associated with gestational diabetes mellitus (GDM). The GSE70493 dataset used for this study was obtained from the Gene Expression Omnibus database. Differentially expressed genes (DEGs) in the placental tissue of women with GDM in relation to the control tissue samples were identified and submitted to protein-protein interaction (PPI) network analysis and subnetwork module mining. Functional enrichment analyses of the PPI network and subnetworks were subsequently carried out. Finally, the integrated miRNA-transcription factor (TF)-DEG regulatory network was analyzed. In total, 238 DEGs were identified, of which 162 were upregulated and 76 were downregulated. Through PPI network construction, 108 nodes and 278 gene pairs were obtained, from which chemokine (C-X-C motif) ligand 9 (CXCL9), CXCL10, protein tyrosine phosphatase, receptor type C (PTPRC), and human leukocyte antigen (HLA) were screened out as hub genes. Moreover, genes associated with the immune-related pathway and immune responses were found to be significantly enriched in the process of GDM. Finally, miRNAs and TFs that target the DEGs were predicted. Four candidate genes (viz., CXCL9, CXCL10, PTPRC, and HLA) are closely related to GDM. miR-223-3p, miR-520, and thioredoxin-binding protein may play important roles in the pathogenesis of this disease.
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ISSN:1477-7827
1477-7827
DOI:10.1186/s12958-019-0546-z