Epigenetic Methylation Changes in Pregnant Women: Bisphenol Exposure and Atopic Dermatitis

Author:

Kim Seung Hwan1ORCID,Yu So Yeon2,Choo Jeong Hyeop2,Kim Jihyun34,Ahn Kangmo34,Hwang Seung Yong56ORCID

Affiliation:

1. Department of Bio-Nanotechnology, Hanyang University, Ansan 15588, Republic of Korea

2. Department of Molecular & Life Science, Hanyang University, Ansan 15588, Republic of Korea

3. Department of Pediatrics, Samsung Medical Center, Sungkyunkwan University School of Medicine, Seoul 06351, Republic of Korea

4. Department of Health Sciences and Technology, Samsung Advanced Institute for Health Sciences & Technology, Seoul 06355, Republic of Korea

5. Department of Medicinal and Life Sciences, Hanyang University, Ansan 15588, Republic of Korea

6. Department of Applied Artificial Intelligence, Hanyang University, Ansan 15588, Republic of Korea

Abstract

Bisphenol is a chemical substance widely used in plastic products and food containers. In this study, we observed a relationship between DNA methylation and atopic dermatitis (AD) in the peripheral blood mononuclear cells (PBMCs) of pregnant women exposed to bisphenol A (BPA) and its alternatives, bisphenol S (BPS) and bisphenol F (BPF). DNA methylation is an epigenetic mechanism that regulates gene expression, which can be altered by environmental factors, and affects the onset and progression of diseases. We found that genes belonging to the JAK-STAT and PI3K-AKT signaling pathways were hypomethylated in the blood of pregnant women exposed to bisphenols. These genes play important roles in skin barrier function and immune responses, and may influence AD. Therefore, we suggest that not only BPA, but also BPS and BPF, which are used as alternatives, can have a negative impact on AD through epigenetic mechanisms.

Funder

Korean Government

Korea Ministry of Environment

Publisher

MDPI AG

Subject

Inorganic Chemistry,Organic Chemistry,Physical and Theoretical Chemistry,Computer Science Applications,Spectroscopy,Molecular Biology,General Medicine,Catalysis

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