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Effects of GDM involves alterations in gene specific DNA methylation

ABSTRACT: Gestational diabetes mellitus(GDM) will bring health issues for offspring. The offspring of diabetic mothers often reveal high birth weight and are prone to have obesity, hypertension and dyslipidemia. It was implied that the phenotype of offspring might be influenced by intrauterine environment and planned in utero already in addition to the genetic influences.‘Programming’ refers to the process whereby a stimulus at a critical window of development has long-term effects. A large body of studies investigated the adverse intrauterine environment was correlated with poor fetal growth and increased risk of Type 2 diabetes in the adulthood. Epigenetic mechanism has been proposed to involve in the link between environmental and nutritional factors and gene expression regulation. DNA methylation is one of the major epigenetic modifications. We hypothesized that DNA methylation changes could participate in the gene expression related to glucose intolerance in the offspring. Furthermore, DNA methylation might also determine the transgenerational disease transmission.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE65779 | GEO | 2015/02/10

SECONDARY ACCESSION(S): PRJNA274993

REPOSITORIES: GEO

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Project description:The prevalence of metabolic syndrome comprising obesity, type 2 diabetes mellitus and cardiovascular disease has been on the rise world-wide in recent years. As non-communicable diseases such as type 2 diabetes mellitus have their roots in prenatal development and conditions such as maternal gestational diabetes (GDM), we aimed to test this hypothesis in primary cells derived from the offspring of GDM mothers compared to control subjects. Methods We have assessed primary umbilical cord derived cells such as human vascular endothelial cells (HUVECs) and Wharton’s jelly derived mesenchymal stem cells (WJMSCs) from both, the offspring of GDM and healthy mothers. We have compared the primary isolates in cell based assays measuring proliferation, mitochondrial oxygen consumption, as well as the ability to support blood vessel growth. We conducted gene expression microarray studies with subsequent pathway analysis and candidate gene validation. Results We observed striking differences between the two groups such as lower metabolic rates and impairment of tube formation in cells with GDM background. HUVECs from subjects with maternal GDM have lower expression of the anti-apoptotic protein BCL-Xl suggesting compromised angiogenic capabilities. Comparative gene expression analysis revealed blood vessel formation as a major pathway enriched in the GDM derived HUVECs with the surface marker CD44 as a significant gene under-expressed in the GDM group. Functional validation of CD44 revealed that it regulates tube formation in HUVECs thereby providing new insights into a novel pathway imprinted in primary umbilical cord derived cells from GDM offspring. Conclusions/interpretation Our data demonstrate that primary cells isolated from the umbilical cord of offspring born to GDM mothers maintain metabolic and molecular imprints of maternal hyperglycemia, which occurred during prenatal development reflecting an enhanced risk for cardiovascular disease later in life.

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Effects of GDM involves alterations in gene specific DNA methylation

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