AI Article Synopsis
- Early life stress (ELS) alters gene expression through epigenetic changes, but its impact during adulthood and across different ages remains unclear.
- A study on adult mice revealed that those exposed to ELS during early life displayed behavioral changes and reduced p11 gene expression, particularly in middle-aged mice as compared to younger ones.
- Findings indicated that, with age, there was a reduction in certain histone modifications and increased DNA methylation at the p11 promoter, showcasing age-dependent effects of ELS on gene regulation.
Article Abstract
Early life stress (ELS) causes long-lasting changes in gene expression through epigenetic mechanisms. However, little is known about the effects of ELS in adulthood, specifically across different age groups. In this study, the epigenetic modifications of p11 expression in adult mice subjected to ELS were investigated in different stages of adulthood. Pups experienced maternal separation (MS) for 3 h daily from postnatal day 1 to 21. At young and middle adulthood, behavioral test, hippocampal p11 expression levels, and levels of histone acetylation and methylation and DNA methylation at the hippocampal p11 promoter were measured. Middle-aged, but not young adult, MS mice exhibited increased immobility time in the forced swimming test. Concurrent with reduced hippocampal p11 levels, mice in both age groups showed a decrease in histone acetylation (AcH3) and permissive histone methylation (H3K4me3) at the p11 promoter, as well as an increase in repressive histone methylation (H3K27me3). Moreover, our results showed that the expression, AcH3 and H3Kme3 levels of p11 gene in response to MS were reduced with age. DNA methylation analysis of the p11 promoter revealed increased CpG methylation in middle-aged MS mice only. The results highlight the age-dependent deleterious effects of ELS on the epigenetic modifications of p11 transcription.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8410943 | PMC |
| http://dx.doi.org/10.1038/s41598-021-89593-7 | DOI Listing |
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