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Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus

Gestational Diabetes Mellitus (GDM) has a high incidence of pregnancy, which seriously affects the life quality of pregnant women and fetal health. DNA methylation is one of the most important epigenetic modification that can regulate the gene expression level, and thus affect the occurrence of vari...

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Autores principales: Zhang, Yan, Zhang, Tiancheng, Chen, Yunyan
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215015/
https://www.ncbi.nlm.nih.gov/pubmed/30389953
http://dx.doi.org/10.1038/s41598-018-34292-z
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author Zhang, Yan
Zhang, Tiancheng
Chen, Yunyan
author_facet Zhang, Yan
Zhang, Tiancheng
Chen, Yunyan
author_sort Zhang, Yan
collection PubMed
description Gestational Diabetes Mellitus (GDM) has a high incidence of pregnancy, which seriously affects the life quality of pregnant women and fetal health. DNA methylation is one of the most important epigenetic modification that can regulate the gene expression level, and thus affect the occurrence of various diseases. Increasing evidence has shown that gene expression changes caused by DNA methylation play an important role in metabolic diseases. Here we explored the mechanisms and biological processes that affect the occurrence and development of GDM through analyzing the gene expression profiles and DNA methylation data of GDM. We detected 24,577 differential CpG sites mapping to 9339 genes (DMGs, differential methylation gene) and 931 differential expressed genes (DEGs) between normal samples and GDM samples. GO (gene ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis of 326 overlapping genes between DMGs and DEGs showed obvious enrichment in terms related to metabolic disorders and immune responses. We identified Oas1, Ppie, Polr2g as possible pathogenic target genes of GDM by combining protein-protein interaction analysis. Our study provides possible targets for early diagnosis of GDM and information for clinical prevention of abnormal fetal development and type 2 diabetes.
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spelling pubmed-62150152018-11-06 Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus Zhang, Yan Zhang, Tiancheng Chen, Yunyan Sci Rep Article Gestational Diabetes Mellitus (GDM) has a high incidence of pregnancy, which seriously affects the life quality of pregnant women and fetal health. DNA methylation is one of the most important epigenetic modification that can regulate the gene expression level, and thus affect the occurrence of various diseases. Increasing evidence has shown that gene expression changes caused by DNA methylation play an important role in metabolic diseases. Here we explored the mechanisms and biological processes that affect the occurrence and development of GDM through analyzing the gene expression profiles and DNA methylation data of GDM. We detected 24,577 differential CpG sites mapping to 9339 genes (DMGs, differential methylation gene) and 931 differential expressed genes (DEGs) between normal samples and GDM samples. GO (gene ontology) and KEGG (Kyoto Encyclopedia of Genes and Genomes) pathway analysis of 326 overlapping genes between DMGs and DEGs showed obvious enrichment in terms related to metabolic disorders and immune responses. We identified Oas1, Ppie, Polr2g as possible pathogenic target genes of GDM by combining protein-protein interaction analysis. Our study provides possible targets for early diagnosis of GDM and information for clinical prevention of abnormal fetal development and type 2 diabetes. Nature Publishing Group UK 2018-11-02 /pmc/articles/PMC6215015/ /pubmed/30389953 http://dx.doi.org/10.1038/s41598-018-34292-z Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Zhang, Yan
Zhang, Tiancheng
Chen, Yunyan
Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title_full Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title_fullStr Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title_full_unstemmed Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title_short Comprehensive Analysis of Gene Expression Profiles and DNA Methylome reveals Oas1, Ppie, Polr2g as Pathogenic Target Genes of Gestational Diabetes Mellitus
title_sort comprehensive analysis of gene expression profiles and dna methylome reveals oas1, ppie, polr2g as pathogenic target genes of gestational diabetes mellitus
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6215015/
https://www.ncbi.nlm.nih.gov/pubmed/30389953
http://dx.doi.org/10.1038/s41598-018-34292-z
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