# Multiomics Screening Identified CpG Sites and Genes That Mediate the Impact of Exposure to Environmental Chemicals on Cardiometabolic Traits

**Authors:** Majid Nikpay

PMC · DOI: 10.3390/epigenomes8030029 · Epigenomes · 2024-07-29

## TL;DR

This study identifies specific CpG sites and genes that link environmental chemical exposure to heart and metabolic health issues.

## Contribution

A novel multiomics workflow is introduced to identify mediating CpG sites and genes using publicly available data.

## Key findings

- Methylation at cg23627948 reduces GNA12 gene expression, increasing body fat percentage.
- cg21153102 methylation affects CHP1 and GCHFR genes, leading to higher diastolic blood pressure.
- HKR1 and CTDNEP1 mediate the effects of B12 supplementation and air pollution on kidney and blood pressure traits.

## Abstract

An understanding of the molecular mechanism whereby an environmental chemical causes a disease is important for the purposes of future applications. In this study, a multiomics workflow was designed to combine several publicly available datasets in order to identify CpG sites and genes that mediate the impact of exposure to environmental chemicals on cardiometabolic traits. Organophosphate and prenatal lead exposure were previously reported to change methylation level at the cg23627948 site. The outcome of the analyses conducted in this study revealed that, as the cg23627948 site becomes methylated, the expression of the GNA12 gene decreases, which leads to a higher body fat percentage. Prenatal perfluorooctane sulfonate exposure was reported to increase the methylation level at the cg21153102 site. Findings of this study revealed that higher methylation at this site contributes to higher diastolic blood pressure by changing the expression of CHP1 and GCHFR genes. Moreover, HKR1 mediates the impact of B12 supplementation → cg05280698 hypermethylation on higher kidney function, while CTDNEP1 mediates the impact of air pollution → cg03186999 hypomethylation on higher systolic blood pressure. This study investigates CpG sites and genes that mediate the impact of environmental chemicals on cardiometabolic traits. Furthermore, the multiomics approach described in this study provides a convenient workflow with which to investigate the impact of an environmental factor on the body’s biomarkers, and, consequently, on health conditions, using publicly available data.

## Linked entities

- **Genes:** GNA12 (G protein subunit alpha 12) [NCBI Gene 2768], CHP1 (calcineurin like EF-hand protein 1) [NCBI Gene 11261], GCHFR (GTP cyclohydrolase I feedback regulator) [NCBI Gene 2644], ZNF875 (zinc finger protein 875) [NCBI Gene 284459], CTDNEP1 (CTD nuclear envelope phosphatase 1) [NCBI Gene 23399]
- **Chemicals:** B12 (PubChem CID 54605677)

## Full-text entities

- **Genes:** GNA12 (G protein subunit alpha 12) [NCBI Gene 2768] {aka HG1M1, NNX3, RMP, gep}, GCHFR (GTP cyclohydrolase I feedback regulator) [NCBI Gene 2644] {aka GFRP, HsT16933, P35}, CTDNEP1 (CTD nuclear envelope phosphatase 1) [NCBI Gene 23399] {aka DULLARD, HSA011916, NET56}, ZNF875 (zinc finger protein 875) [NCBI Gene 284459] {aka HKR1}
- **Chemicals:** Chemicals (-), lead (MESH:D007854), perfluorooctane sulfonate (MESH:C076994), Organophosphate (MESH:D010755), B12 (MESH:C034730)

## Full text

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## Figures

5 figures with captions in the complete paper: https://tomesphere.com/paper/PMC11348123/full.md

## References

32 references — full list in the complete paper: https://tomesphere.com/paper/PMC11348123/full.md

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Source: https://tomesphere.com/paper/PMC11348123