Altered expression of PGC-1 α and PDX1 and their methylation status are associated with fetal glucose metabolism in gestational diabetes mellitus

Wang, Lizhen; Fan, Hailing; Zhou, Ludan; Wu, Yanjun; Lu, Hongping; Luo, Jing

doi:10.1016/j.bbrc.2018.05.010

Cited by 27 publications

(27 citation statements)

References 34 publications

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“…Changes in the promoter DNA methylations and miRNA expression play vital roles in pregnancy-related diseases by up-or down-regulating gene expression. 26,27 DNA methylation pattern and miRNA expression alterations can serve as useful biomarkers to distinguish GDM from normal samples, 27,28 which would be used for clinical diagnosis, assessment of treatment and diagnosis. 29 In the TA B L E 1 Ten chemicals were predicted as putative therapeutic agents for GDM 33,34 Notably, overall 18 genes were controlled by more than one miRNAs, which may be the intersection of multiple miRNA regulation.…”

Section: Discussionmentioning

confidence: 99%

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Zhu

Shen

Liu

et al. 2020

J Cellular Molecular Medi

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Section: Discussionmentioning

confidence: 99%

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Zhu

Shen

Liu

et al. 2020

J Cellular Molecular Medi

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“…GDM pathogenesis has previously been related to alterations in placental gene expression and DNA methylation . However, the mechanism through which placental dysfunction occurs is extremely complicated and remains unclear.…”

Section: Discussionmentioning

confidence: 99%

Identification of hub‐methylated differentially expressed genes in patients with gestational diabetes mellitus by multi‐omic WGCNA basing epigenome‐wide and transcriptome‐wide profiling

Chen

Yan

Han

et al. 2019

J of Cellular Biochemistry

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Gestational diabetes mellitus (GDM), defined as dysglycaemia that is detected during pregnancy for the first time, has become a global health burden. GDM was found to be correlated to epigenetic changes, which would cause abnormal expression of placental genes. In the present study, we performed multi-omic weighted gene coexpression network analysis (WGCNA) to systematically identify the hub genes for GDM using both epigenome-and transcriptomewide microarray data. Two microarray datasets (GSE70493 and GSE70494) were downloaded from the Gene Expression Omnibus (GEO) database. GEO2R was used to screen differentially expressed genes (DEGs) and differentially methylated genes (DMGs) between normal and GDM samples, separately. The results of WGCNA found that 15 modules were identified and the MEblack module had a significantly negative correlation with GDM (r = −.28, P = .03). GO enrichment analysis by BinGO of the MEblack module showed that genes were primarily enriched for the presentation of antigen processing, regulation of interferon-α production and interferon-γ-mediated signaling pathway. By comparing the DEGs, DMGs and hub genes in the coexpression network, we identified five hypermethylated, lowly expressed genes (ABLIM1, GRHL1, HLA-F, NDRG1, and SASH1) and one hypomethylated, highly expressed gene (EIF3F) as GDM-related hub DMGs. Moreover, the expression levels of ABLIM1, GRHL1, HLA-F, NDRG1, and SASH11 in the GDM patients and healthy controls were validated by a real-time quantitative polymerase chain reaction. Finally, gene set enrichment analysis showed that the biological function of cardiac muscle contraction was enriched for four GDM-related hub DMGs (ABLIM1, GRHL1, NDRG1, and SASH1). Analysis of this study revealed that dysmethylated hub genes in GDM placentas might affect the placental function and thus, take part in GDM pathogenesis and fetal cardiac development. K E Y W O R D S epigenome, gestational diabetes mellitus, transcriptome, WGCNA

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“…It is expressed during the early stage of β-cell development and is crucial to its function [18]. Evidence shows that both genetic and acquired reductions in Pdx1 expression may lead to type 2 diabetes, β-cell dysfunction, and compromised islets compensation to insulin resistance in human and animal models alike [19][20][21].…”

Section: Discussionmentioning

confidence: 99%

“…Adult post-diabetes-onset methylation may cause permanent silencing of Pdx1 expression. Likewise, an abnormal intrauterine environment may lead to epigenetic alterations that regulate the main genes associated with β-cell development, leaving Pdx1 expression permanently lowered within β cells [20].…”

Section: Discussionmentioning

confidence: 99%

Exposure to PM_2.5 during pregnancy or lactation increases methylation while reducing the expression of Pdx1 and NEUROG3 in mouse pancreatic islets

Lima

Boico

Peruca

et al. 2019

Preprint

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Air pollution is comprised of several substances, including particulate matter (PM). Exposure to air pollution may trigger alterations in DNA methylation thus modifying gene expression patterns. This phenomenon is likely to mediate the relationship between exposure to air pollution and adverse health effects. The purpose of this study was analyzing the effects of exposure to PM 2.5 during pregnancy or lactation and whether it would cause multigenerational epigenetic alterations in the promoter region of the genes Pdx1 and NEUROG3 within mouse pancreatic islets. Our results show that maternal exposure to PM 2.5 led to an elevation in blood glucose levels within the two following generations (F1 and F2). There was also an increase in DNA methylation in the aforementioned promoter regions accompanied by reduced gene expression in generations F1 and F2 upon F0 exposure to PM 2.5 during pregnancy. These data suggest that maternal exposure to PM 2.5 from air pollution, particularly during pregnancy, may lead to a multigenerational and lifelong negative impact on glucose homeostasis mediated by an increase in DNA methylation within the promoter region of the genes Pdx1 and NEUROG3 in pancreatic islets.

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Altered expression of PGC-1 α and PDX1 and their methylation status are associated with fetal glucose metabolism in gestational diabetes mellitus

Cited by 27 publications

References 34 publications

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Identification of hub‐methylated differentially expressed genes in patients with gestational diabetes mellitus by multi‐omic WGCNA basing epigenome‐wide and transcriptome‐wide profiling

Exposure to PM_2.5 during pregnancy or lactation increases methylation while reducing the expression of Pdx1 and NEUROG3 in mouse pancreatic islets

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Altered expression of PGC-1 α and PDX1 and their methylation status are associated with fetal glucose metabolism in gestational diabetes mellitus

Cited by 27 publications

References 34 publications

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Epigenetic alternations of microRNAs and DNA methylation contribute to gestational diabetes mellitus

Identification of hub‐methylated differentially expressed genes in patients with gestational diabetes mellitus by multi‐omic WGCNA basing epigenome‐wide and transcriptome‐wide profiling

Exposure to PM2.5 during pregnancy or lactation increases methylation while reducing the expression of Pdx1 and NEUROG3 in mouse pancreatic islets

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Exposure to PM_2.5 during pregnancy or lactation increases methylation while reducing the expression of Pdx1 and NEUROG3 in mouse pancreatic islets