DNA methylation of genes that mediate autophagosome formation contributes to iodine-induced autoimmune thyroiditis: A population-based study conducted at regions with different iodine levels in China.

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Tác giả: Yao Chen, Yun Chen, Mengxue Du, Haiyan Gao, Yanhong He, Jinjin Liu, Lixiang Liu, Bingxuan Ren, Hongmei Shen, Siyuan Wan, Xianhao Wu, Zheng Zhou

Ngôn ngữ: eng

Ký hiệu phân loại: 627.12 Rivers and streams

Thông tin xuất bản: Germany : International journal of hygiene and environmental health , 2025

Mô tả vật lý:

Bộ sưu tập: NCBI

ID: 199656

 PURPOSE: Autoimmune thyroiditis (AIT) results from a combination of genetic predispositions and environmental factors. This study aims to examine the methylation patterns of genes that mediate autophagosome formation (MAF) between AIT patients and controls from areas with different water iodine levels. METHODS: A protein-protein interaction (PPI) network was constructed to explore the interactions of autophagy-related genes (ARGs). The MCODE plugin in Cytoscape software identified two functional epigenetic modules. We included 176 AIT cases from regions with varying water iodine concentrations and matched controls at a 1:1 ratio. The MethylTarget™ assay was employed to assess DNA methylation changes in six MAF-related genes and analyzed the association between iodine levels and epigenetic modifications. RESULTS: Significant methylation differences were observed in 11 targets with 75 CpG sites on MAF-related genes between AIT patients and controls (P <
  0.05). Methylation levels were generally lower in AIT patients. A negative correlation was found between the methylation status of PRKAB1_36 and urinary iodine concentration (UIC) (r CONCLUSION: Environmental water iodine concentration influences the DNA methylation status of MAF-related genes. Hypomethylated targets and sites in these genes were identified, and the relative mRNA expression levels of these genes were significantly increased in AIT cases from regions with a history of prolonged iodine deficiency followed by iodine supplementation.
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