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- W4225434589 abstract "Developmental arsenic exposure has been associated with cognitive deficits in epidemiological studies, but the underlying mechanisms remain poorly understood. Here, we establish a mouse model of developmental arsenic exposure exhibiting deficits of recognition and spatial memory in the offspring. These deficits are associated with genome-wide DNA hypomethylation and abnormal expression of cognition-related genes in the hippocampus. Arsenic atoms directly bind to the cysteine-rich ADD domain of DNA methyltransferase 3A (DNMT3A), triggering ubiquitin- and proteasome-mediated degradation of DNMT3A in different cellular contexts. DNMT3A degradation leads to genome-wide DNA hypomethylation in mouse embryonic fibroblasts but not in non-embryonic cell lines. Treatment with metformin, a first-line antidiabetic agent reported to increase DNA methylation, ameliorates the behavioral deficits and normalizes the aberrant expression of cognition-related genes and DNA methylation in the hippocampus of arsenic-exposed offspring. Our study establishes a DNA hypomethylation effect of developmental arsenic exposure and proposes a potential treatment against cognitive deficits in the offspring of pregnant women in arsenic-contaminated areas." @default.
- W4225434589 created "2022-05-05" @default.
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- W4225434589 date "2022-04-04" @default.
- W4225434589 modified "2023-10-16" @default.
- W4225434589 title "Developmental arsenic exposure impairs cognition, directly targets DNMT3A, and reduces DNA methylation" @default.
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- W4225434589 doi "https://doi.org/10.15252/embr.202154147" @default.
- W4225434589 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/35373418" @default.
- W4225434589 hasPublicationYear "2022" @default.
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