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Sexually dimorphic methylation of CD3+ T-lymphocyte DNA in offspring of overweight and obese mothers in a high risk, minority population in the Bronx

ABSTRACT: Maternal obesity impacts the health of offspring, increasing the risk of developing obesity and/or other metabolic dysregulation in childhood or later in life. Using a genome-wide methylation assay, we identified sex-dependent dysregulation of the methylome of CD3+ T-lymphocytes, a cell type that plays an important role in obesity and inflammatory diseases, in newborn offspring of overweight and obese mothers. Furthermore, the differentially methylated loci were targeted to regulatory regions of the genome, in imprinted genes and genes identified from GWAS as being related to type 2 diabetes and obesity.

ORGANISM(S): Homo sapiens

PROVIDER: GSE94729 | GEO | 2020/02/07

REPOSITORIES: GEO

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Project description:Background and aims: Youth populations with overweight/obesity (OW/OB) exhibit heterogeneity in cardiometabolic health phenotypes (e.g. fasting glucose, serum triglycerides, etc.). The underling mechanisms for those differences are still unclear. This study aimed to analyze the whole blood transcriptome profile (RNA-seq) of children with metabolic healthy overweight/obesity (MHO) and metabolic unhealthy overweight/obesity (MUO) phenotypes. Methods: 27 children with OW/OB (10.14 ± 1.3 years, 59% boys) from the ActiveBrains project were included. MHO was defined as having none of the following criteria for metabolic syndrome: elevated fasting glucose, high serum triglycerides, low high-density lipoprotein cholesterol, and high systolic or diastolic blood pressure, while MUO was defined as presenting one or more of these criteria. Inflammatory markers interleukin-1β (IL-1β), IL-6, tumor necrosis factor-α (TNF-α), epidermal growth factor (EGF) and, vascular endothelial growth factor A (VEGF) were additionally determined. Total-blood RNA was analyzed by 5’-end RNA sequencing. Two different bioinformatics approaches were performed: 1) Differential gene expression analyses using Limma R/Bioconductor software package (analyses adjusted by sex and maturational status) and 2) weighted gene coexpression network analyses (WGCNA). Results: Children with MHO had lower values of pro-inflammatory cytokines TNF-α and IL-6 compared to MUO (p < 0.05). 40 genes were differentially expressed (FDR < 0.05) in children with MHO compared to MUO. WGCNA analysis identified 23 gene coexpression modules (i.e. clusters of genes) with low preservation (Zsummary < 2) in children with MHO compared to MUO. Differential and WGCNA gene expression patterns identified 32 genes linked to metabolism, mitochondrial and immune functions. Conclusions: Whole blood transcriptome analysis revealed a distinct pattern of gene expression in children with MHO compared to MUO children. The identified gene expression patterns related to metabolism, mitochondrial and immune functions can promote a better understanding of cardiovascular disease prognosis in individuals with MHO.

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Sexually dimorphic methylation of CD3+ T-lymphocyte DNA in offspring of overweight and obese mothers in a high risk, minority population in the Bronx

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